mEq Potassium Research Articles

224: ALTERNATIVE MANAGEMENT OF DIABETIC KETOACIDOSIS DUE TO REFRACTORY HYPOKALEMIA

Introduction: In a hypoglycemic state, potassium levels are falsely elevated due to potassium shifting extracellularly. Once insulin is initiated, potassium will reverse, returning intracellularly, and leading to a lower potassium level. It is this reason that the standard protocol of diabetic ketoacidosis (DKA) treatment is to not begin insulin until potassium is replenished above a designated level. Below we present a patient with DKA that required treatment outside of standard protocol due to refractory hypokalemia. Description: The patient is a 25-year-old male that presented to the emergency department (ED) with elevated glucose for the past few weeks. He is a type-2 diabetic, controlled with diet and exercise for the last year. Prior to which, he had been on insulin. The only exacerbating factor he can think of is receiving the J&J vaccine around the same time. Other associated symptoms are difficulty breathing, abdominal pain, mild nausea, but no vomiting. In the ED, he was found to be in DKA with labs significant for severe acidosis and critical hypokalemia of 1.6 mmol/L. A central line was placed and potassium repletion began prior to initiating insulin drip, with plan to start insulin once potassium corrected. Following aggressive potassium repletion with up to 40 mEq per hour, it persistently remained below 3 mmol/L. Thus, it was decided to start the patient on the lowest rate of the insulin drip at 0.02 units/kg/hr until his potassium rose above 3.3 mmol/L as per our protocol. While being on the insulin drip, he was also receiving 20 mEq potassium hourly via IV, 40 mEq orally every four hours, with frequent basic metabolic profiles every two hours. The patient remained on the insulin drip for three days until he was finally able to be transitioned to long-acting insulin, 73-hours after admission. Discussion: The treatment of refractory hypokalemia in the setting of DKA is intricate. Insulin, while imperative for the treatment of DKA, can worsen hypokalemia, therefore sequence of medication administration is important in treatment. It is important for providers to recognize and identify the side effects of these treatments. In this case, multidisciplinary rounds were crucial in both monitoring and replacing potassium while on an insulin drip.

Myocardial protection with glucose-insulin potassium in patients with acute coronary syndromes requiring coronary artery bypass grafting: A case series

Emergent cardiac surgery in patients with acute coronary syndrome (ACS) is always a challenging task for surgeons, anesthesiologists and patients. As “time is muscle,” early revascularization by percutaneous coronary intervention (PCI) has been largely advocated to salvage myocardial ischemic cells. In cases judged not suitable for PCI, on-pump coronary artery bypass grafting (CABG) is indicated with cardioplegic arrest and eventually anesthetic preconditioning to enhance myocardial protection. In these high-risk emergent procedures, adjuvant interventions to cardioplegic arrest are aimed to maximize the chance of cardiac functional recovery. Although the infusion of glucose-insulin-potassium (GIK) has demonstrated interesting cardioprotective effects in animal models of myocardial ischemia and in patients undergoing elective cardiac surgery, this cardioprotective strategy has not yet been adopted largely and has been ignored so far in emergent myocardial revascularization procedures. In this case series, we describe the effects of GIK on left ventricular performance assessed by transesophageal echocardiography in four patients with ACS who required emergent CABG surgery. The GIK solution of 20 g glucose, 20 UI insulin and 10 mEq potassium chloride was infused twice over 30 min, first after anesthesia induction and later after aortic unclamping. The systolic performance was assessed after anesthesia induction and after each GIK infusion using the 3D left ventricular ejection fraction, as well as the global longitudinal and circumferential strain. The diastolic function was assessed based on mitral inflow patterns (E-and A-waves) as well as flow propagation velocity.

Estimation of Potassium Changes Following Potassium Supplements in Hypokalemic Critically Ill Adult Patients-A Patient Personalized Practical Treatment Formula.

Hypokalemia is common among critically ill patients. Parenteral correction of hyperkalemia depends on dosages and patient characteristics. Our aims were to assess changes in potassium levels following parenteral administration, and to derive a formula for predicting rises in serum potassium based on patient characteristics. We conducted a population-based retrospective cohort study of adults hospitalized in a general intensive care unit for 24 h or more between December 2006 and December 2017, with hypokalemia. The primary exposures were absolute cumulative intravenous doses of 20, 40, 60 or 80 mEq potassium supplement. Adjusted linear mixed models were used to estimate changes in serum potassium. Of 683 patients, 422 had mild and 261 moderate hypokalemia (serum potassium 3.0–3.5 mEq/L and 2.5–2.99 mEq, respectively). Following doses of 20–80 mEq potassium, serum potassium levels rose by a mean 0.27 (±0.4) mEq/L and 0.45 (±0.54) mEq/L in patients with mild and moderate hypokalemia, respectively. Changes were associated with creatinine level, and the use of mechanical ventilation and vasopressors. Among critically ill patients with mild to moderate hypokalemia, increases in serum potassium after intravenous potassium supplement are influenced by several clinical parameters. We generated a formula to predict the expected rise in serum potassium based on clinical parameters.

Thyrotoxic Periodic Paralysis

Thyrotoxic Periodic Paralysis (TPP) is an emergency associated with flaccid paralysis in which the paralysis is reversible with prompt potassium replacement and the attacks are terminated when hyperthyroidism is cured. Timely diagnosis and treatment are therefore prudent. While managing patients with flaccid paralysis, physicians should be aware of TPP as potential etiology and investigate history to identify the triggering factors and provide timely and cautious treatment with replacement of potassium, further addressing permanent approaches to treating thyrotoxicosis to prevent future recurrences of TPP. We report a clinical scenario of a patient who experienced TPP.22-year-old male, laying down at home at around 1:45pm developed sudden onset bilateral lower extremity weakness and was unable to stand up. His weakness was associated with thigh pain with exertion. He was eventually able to walk a few steps, but then fell onto his knees. He reported having a carbohydrate rich lunch at noon. Notably, patient underwent surgery under general anesthesia for a deviated nasal septum the day before. His neurological examination was remarkable for giveaway proximal lower extremity weakness involving only select muscle groups. Examination and CT/CTA of head and neck findings was not consistent with acute stroke. Myopathy secondary to electrolyte imbalance, drug/toxin, infection, or inflammatory disorders, myelopathy and myasthenia gravis were considered in the differential. Labs revealed suppressed TSH <0.01uIU/mL, elevated FT4 of 6ng/dL and low serum potassium of 2.6mmol/L. CT scan of the neck revealed enlarged thyroid gland and thymic enlargement. Patient was given intravenous bolus of potassium chloride 20 mEq and serum potassium normalized in 4 hours to 3.8mmol/L. His lower extremity weakness resolved within 3hours of potassium replacement. The next day his serum potassium was 5.2mmol/L. His thyroid stimulating immunoglobulin index was elevated at 1.4 (normal <1.3). He was started on propranolol, methimazole and advised to return to the endocrinology clinic to discuss permanent treatment options for hyperthyroidism to prevent TPP. Reviewing his prior medical history, he was diagnosed with Graves’ disease 5 months prior to the emergency room evaluation and was started on methimazole. He took methimazole for 2 months and did not return to follow up until the occurrence of TPP. He did not experience symptoms of hyperthyroidism in the interim. Discussion: TPP is a rare disorder with a prevalence of 0.1-0.2% in North America. TPP commonly affects Asian and Latin Americans males. The episodes of TPP are influenced by genetic, environmental, and ethnic factors. Common environmental triggers include carbohydrate rich meals, rest after intense physical exertion, fever, infection, trauma, emotional stress, and smoking. Thymic hyperplasia has also been reported to be associated with hypokalemic periodic paralysis. Clinical Presentation: The motor weakness tends to affect proximal lower extremities as noted in our patient’s presentation and is usually associated with hyporeflexia and is painless. Cardiac arrhythmias due to hypokalemia are rare, though ventricular fibrillation have been reported, and respiratory failure requiring mechanical ventilation is a possibility. Pathophysiology: TPP has been thought to be a channelopathyassociated with increased Na+–K+ ATPase activity and loss of function mutation of the Kir 2.6 potassium efflux channel resulting in intracellular pooling of potassium and transient hypokalemia. The attacks are stimulated by thyroid hormone excess and/or hyperadrenergic activity and hyperinsulinemia, most commonly due to carbohydrate load or intravenous fluids containing dextrose. Treatment should include:1.Potassium supplementation to reverse paralysis and prevent life threatening cardiac arrhythmias. Care must be taken to not over replace potassium, as it could result in hyperkalemia when potassium channels revert to functioning normally.2.Propranolol, a non-selective betablocker works by blocking the thyroid hormone mediated adrenergic overstimulation of the Na-K ATPase channel, there by limiting the intracellular pooling of potassium.3.Definitive treatment of thyrotoxicosis should be offered. Studies comparing various modalities of treatment of thyrotoxicosis in the setting of TPP indicate permanent treatment with either radioactive iodine or thyroidectomy are often successful in preventing recurrence of TPP, as relapse events are higher in treatment with antithyroid drugs. Caution should be taken to prevent surge of thyroid hormone release following radioactive iodine treatment, as this can trigger TPP. Higher doses of radioactive iodine might be required to render hypothyroidism and prevent TPP recurrences. There is one case report of hypokalemic periodic paralysis associated with thymic hyperplasia that was treated with thymectomy. Our patient had multiple triggers leading to periodic paralysis, including a prior untreated Graves’ disease due to non-adherence to treatment during COVID-19 pandemic, general anesthesia for nasal septal surgery the day before presenting with TPP, having a carbohydrate rich meal one hour before the episode, and thymic enlargement on neck CT scan. He responded well to potassium replacement, and propranolol. He was started on methimazole and offered permanent treatment options to address hyperthyroidism.

Primary Hyperaldosteronism in Pregnancy: A Case Report

Background: Primary aldosteronism (PA) is a renin-independent hypersecretion of aldosterone that remains an underdiagnosed etiology of hypertension. Less than 50 cases of primary hyperaldosteronism in pregnancy have been reported in literature that are associated with pregnancy complications including preeclampsia. Clinical Case: A 41-year-old female G9P4 at 32 weeks gestation was admitted for suspected preeclampsia due to elevated blood pressure during a routine prenatal visit. Her comorbidities include type 2 diabetes, uncontrolled hypertension, and preeclampsia in a previous pregnancy. Home medications included Lisinopril 10 mg once daily which was discontinued upon pregnancy and switched to Labetalol 400 mg twice daily and Nifedipine ER 30 mg daily. She was on a total of 220 units of insulin daily.On presentation, patient complained of anxiety but denied any headache, nausea, visual disturbances, chest pain, palpitations, muscle cramps, or fatigue. Her blood pressure was 180/100 mmHg with heat rate of 73. Laboratory values was notable for potassium: 2.8 mmol/L (n 3.5–5 mmol/L), bicarbonate: 28 mmol/L (n 24–31 mmol/L), and magnesium: 1.4 mEq/L (n 1.3–1.9 mEq/L). Liver function test and platelet count were normal. Spot protein-creatinine ratio was 0.3 (n 0–0.2). ECG was normal sinus rhythm with a heart rate of 82 without decreased T wave amplitude or U waves. She received three doses of oral 40 mEq potassium chloride over twelve hours and potassium level post repletion was 3.0 mmol/L.Initially, her hypokalemia was attributed to high insulin dose requirements. Despite down titration of insulin, patient continued to have hypokalemic episodes (nadir 2.7 mmol/L) refractory to oral and parenteral potassium supplementation. She remained hypertensive despite Labetalol 600 mg every 8 hours, Nifedipine ER 30 mg every 12 hours, with as needed hydralazine 10 mg IV pushes, and underwent urgent cesarean delivery. Uncontrolled hypertension persisted postpartum with recurrent episodes of hypokalemia. Further investigations revealed a plasma aldosterone concentration (PAC) and plasma renin activity (PRA) levels of 43.5 ng/dL (n <10 ng/dL) and 1.67 ng/mL/hr (n 0.17–5.38 ng/mL/hr) respectively, potassium at time of testing was 3.6 mmol/L. PAC to PRA ratio was greater than 20:1 with an absolute PAC greater than 15 ng/dL, which is highly suggestive of PA. Conclusion: We present a case of suspected PA with spontaneous hypokalemia potentially masked by the use of ACE inhibitors uncovered during pregnancy. Given the changes to the renin-angiotensin-aldosterone system (RAAS) during pregnancy, the diagnosis of PA is difficult to establish during gestation. Still, little is known on how to optimally treat these patients. Reference: Morton, A., 2015. Primary Aldosteronism and Pregnancy. Pregnancy and hypertension. An International Journal of Women’s Cardiovascular Health, Volume 5 Issue 4, 259–262.

Correcting hypophosphataemia in a paediatric patient with Sanjad–Sakati syndrome through a single oral dose of potassium phosphate intravenous solution

Sanjad–Sakati syndrome is an autosomal recessive disorder that is quite common in Kuwait. Among a wide range of complications in Sanjad–Sakati syndrome patients is the vulnerability to infections and subsequent hypophosphataemia. Hypophosphataemia is a metabolic alteration that contributes to numerous consequences such as cardiac arrhythmia. Therefore, if hypophosphataemia is left unresolved, it may culminate in death. A 20-month-old boy of 2.5 kg body weight diagnosed with Sanjad–Sakati syndrome was initially admitted to the paediatric intensive care unit after recovering from COVID-19, and then shifted to the general ward. He was diagnosed with recurrent pneumonia and urinary tract infection. After 9 days, the patient showed severe hypophosphataemia with serum phosphate concentration reaching 0.33 mmol/L. Despite the availability of potassium phosphate intravenous solution, it was difficult to administer potassium phosphate intravenously because of the small body size and low body weight of the patient. Therefore, 0.6 mL potassium phosphate containing 2.4 mEq of potassium and 5.3 mEq of phosphate was administered through a nasogastric tube. The patient showed rapid response after a single dose through the nasogastric tube. Such an intervention in Sanjad–Sakati syndrome patients shows possible advantages of shifting drug administration from intravenous to oral route that includes a convenient route of administration, whether in the intensive care unit or in the general ward. Moreover, shifting drug administration from the intravenous to oral route overcomes the risk of cannula-induced infection and reduces nurses’ workload.

Correcting hypokalaemia in a paediatric patient with Bartter syndrome through oral dose of potassium chloride intravenous solution

Bartter syndrome is a rare autosomal recessive disorder characterized by hypokalaemia. Hypokalaemia is defined as low serum potassium concentration ˂3.5 mmol/L, which may lead to arrhythmia and death if left untreated. The aim of this case report was to normalize serum potassium concentration without the need for intravenous intervention. A 5-month-old male of 2.7 kg body weight diagnosed with Bartter syndrome was admitted to the general paediatric ward with acute severe hypokalaemia and urinary tract infection. The main challenge was the inability to administer drugs through intravenous route due to compromised body size. Therefore, we shifted the route of administration to the nasogastric tube/oral route. A total of 2 mL of concentrated intravenous potassium chloride (4 mEq potassium) were dissolved in distilled water and administered through nasogastric tube. Serum potassium concentration was rapidly normalized, which culminated in patient discharge. In conclusion, shifting drug administration from intravenous to oral route in a paediatric patient with Bartter syndrome includes numerous advantages such as patient convenience, minimized risk of cannula-induced infection, and reduced nurse workload.

Assessment of Hypokalemia and Clinical Characteristics in Patients With Coronavirus Disease 2019 in Wenzhou, China

Severe acute respiratory syndrome coronavirus 2 has caused a global outbreak of coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 binds angiotensin-converting enzyme 2 of the rennin-angiotensin system, resulting in hypokalemia. To investigate the prevalence, causes, and clinical implications of hypokalemia, including its possible association with treatment outcomes, among patients with COVID-19. This cohort study was conducted at Wenzhou Central Hospital and Sixth People's Hospital of Wenzhou, Wenzhou, China, from January 11, 2020, to February 15, 2020. Participants included patients who received a diagnosis of COVID-19 according to the criteria issued by the Chinese Health Bureau and were admitted to the hospital. The patients were classified as having severe hypokalemia (plasma potassium <3 mmol/L), hypokalemia (plasma potassium 3-3.5 mmol/L), and normokalemia (plasma potassium >3.5 mmol/L). The clinical features, therapy, and outcomes were compared between the 3 groups. Data analysis was conducted in March 2020. The patients were given general support and antiviral therapy. Their epidemiological and clinical features were collected. The prevalence of hypokalemia and response to treatment with potassium supplements were measured by analyzing plasma and urine potassium levels. One hundred seventy-five patients (87 female patients [50%]; mean [SD] age, 45 [14] years) were classified as having severe hypokalemia (31 patients [18%]), hypokalemia (64 patients [37%]), and normokalemia (80 patients [46%]). Patients with severe hypokalemia had statistically significantly higher body temperature (mean [SD], 37.6 °C [0.9 °C]) than the patients with hypokalemia (mean [SD], 37.2 °C [0.7 °C]; difference, 0.4 °C; 95% CI, 0.2-0.6 °C; P = .02) and the patients with normokalemia (mean [SD], 37.1 °C [0.8 °C]; difference, 0.5 °C; 95% CI, 0.3-0.7 °C; P = .005). Patients with higher levels of hypokalemia also had higher creatine kinase levels (severe hypokalemia, mean [SD], 200 [257] U/L [median, 113 U/L; interquartile range {IQR}, 61-242 U/L]; hypokalemia, mean [SD], 97 [85] U/L; and normokalemia, mean [SD], 82 [57] U/L), higher creatine kinase-MB fraction (severe hypokalemia, mean [SD], 32 [39] U/L [median, 14 U/L; IQR, 11-36 U/L]; hypokalemia, mean [SD], 18 [15] U/L; and normokalemia, mean [SD], 15 [8] U/L), higher lactate dehydrogenase levels (mean [SD], severe hypokalemia, 256 [88] U/L; hypokalemia, 212 [59] U/L; and normokalemia, 199 [61] U/L), and higher C-reactive protein levels (severe hypokalemia, mean [SD], 29 [23] mg/L; hypokalemia, mean [SD], 18 [20] mg/L [median, 12, mg/L; IQR, 4-25 mg/L]; and normokalemia, mean [SD], 15 [18] mg/L [median, 6 U/L; IQR, 3-17 U/L]). Of 40 severely and critically ill patients, 34 (85%) had hypokalemia. Patients with severe hypokalemia were given potassium at a dose of 40 mEq per day, for a total mean (SD) of 453 (53) mEq potassium chloride, during the hospital stay. The patients responded well to potassium supplements as they recovered. The correction of hypokalemia is challenging because of continuous renal potassium loss resulting from the degradation of angiotensin-converting enzyme 2. The high prevalence of hypokalemia among patients with COVID-19 suggests the presence of disordered rennin-angiotensin system activity, which increases as a result of reduced counteractivity of angiotensin-converting enzyme 2, which is bound by severe acute respiratory syndrome coronavirus 2.

Augmented sympathetic neural responses to a cold pressor test during salt loading in healthy premenopausal women

BackgroundExcessive salt intake is considered a risk factor for the development of hypertension. Previous studies have demonstrated that augmented neural and pressor responses to a cold stimulus are associated with an increased risk of hypertension. This study aimed to determine whether salt loading impacts sympathetic neural responses during the cold pressor test (CPT) in healthy young and middle‐aged women.MethodsNine healthy premenopausal women [42±3 (SD) yr] were given a standardized isocaloric high‐salt (HS; 250 mEq sodium, 100 mEq potassium, and 1000 mg calcium per day) or low‐salt diet (LS; 50 mEq sodium, 100 mEq potassium, and 1000 mg calcium per day) for 1 week each (~2‐month apart with the order randomized), while water intake was ad libitum. Twenty‐four‐hour urine was collected and laboratory testing was performed following each HS and LS period in the mid‐luteal phase of the menstrual cycle. Subjects were in the supine position and beat‐by‐beat BP, heart rate (HR) and muscle sympathetic nerve activity (MSNA) were measured during baseline, 2‐minute CPT, and 3‐minute recovery. Blood sample was taken to calculate the change in plasma and blood volume by using the Dill’s equation. Salt sensitive was defined as more than 10% changes in mean arterial pressure between HS and LS, and below this cutoff was defined as non‐salt‐sensitive.ResultAll subjects were non‐salt‐sensitive (salt sensitivity range: −7.78 to 6.49%). Urine osmolality and 24‐h urine sodium were higher during HS than LS (572±174 vs. 443±153 mOs/kg and 150.8±72.1 vs. 65.2±38.5 mmol/day, both P&lt;0.05). Plasma and blood volume increased by 6.9±1.8% (p=0.006) and 4.3±1.2% (p=0.008) in HS compared with LS. Baseline systolic and diastolic BP (103±12 vs. 105±10 mmHg and 59±6 vs. 69±9 mmHg), HR (66±10 vs. 63±9 bpm), or MSNA (burst frequency: 14±11 vs. 16±10 bursts/min and total activity: 156±118 vs.184±115 a.u./min) did not differ between HS and LS (all P&gt;0.05). Systolic and diastolic BP and HR increased during the CPT (all P&lt;0.001) with no salt effects (all P&gt;0.05). MSNA increased during the CPT in both conditions (both P&lt;0.001), but the increases in burst frequency and total activity were greater during HS than LS (Δ burst frequency: 26±20 vs. 14±15 bursts/min and Δ total activity: 644±480 vs.368±402 a.u./min, P=0.042 and 0.002 for interaction, as figure ).ConclusionSalt loading augments sympathetic neural responses to the cold pressor stimulus with no significant impact on blood pressure responses in healthy premenopausal non‐salt‐sensitive women. Whether similar results can be obtained in salt‐sensitive women remains to be determined.Support or Funding InformationThe Harry S. Moss Heart Trust awardChanges (Δ) from baseline in muscle sympathetic nerve activity (MSNA) burst frequency, total activity, mean arterial pressure and heart rate during cold pressor test (CPT) and recovery in high salt and low salt diet. Values are means ± SD. *, high salt vs low salt at P&lt;0.05.Figure 1

Evaluation of the safety and efficacy of the central venous administration of potassium chloride including the measurement of intracardiac potassium concentrations

This study examined the safety and efficacy of the intravenous administration of 20 mEq potassium chloride (KCl) dissolved in a 100 cc 5% dextrose in sterile water bolus over 1 hour through a subclavian central vein catheter in critical care unit patients for the treatment of low and low to normal serum potassium concentrations. We studied seven patients with morning serum potassium between 2.4 and 3.6 mEq/L who had intravenous KCl boluses ordered by their treating physician. Intracardiac and peripheral venous potassium levels were obtained before, during, and after infusion. Holter and electrocardiogram assessment of rhythm, supraventricular and ventricular ectopy, and electrical intervals were recorded before, during, and after the intravenous KCl bolus. The cardiac rhythm, heart rates, and electrocardiographic intervals remained unchanged throughout the infusion and postinfusion phases. In six of the seven patients, there was no new or worsening supraventricular or ventricular ectopy temporally related to the infusion. Postinfusion potassium levels increased in all patients, with an average peripheral vein serum potassium increase of 0.4 mEq/L. In conclusion, within the limitations of our sample size, our study demonstrated the safety and efficacy of the central venous infusion of 20 mEq KCl in 100 cc 5% dextrose in sterile water administered over 1 hour.

Influence of the type of amino acids in the formation of precipitates of copper and sulphur in parenteral nutrition.

Objective: we found a black precipitate during the infusion of a parenteral nutrition without lipids. The objective of this study is to check the composition of the precipitate and the influence of the type of amino acids in its formation. Methods: four PN bags were prepared with the following composition: 1 l of amino acids solution, 150 g glucose, 60 mEq potassium, 217 mEq chloride, 105 mEq sodium, 15 mEq magnesium, 15 mEq calcium, 18.63 mmol phosphorus and trace elements (Addamel®). Each bag was prepared using a different type of amino acids solution with different amount of cysteine per litre: Tauramin® 10% (0.5 g/l), Primene® 10% (1.89 g/l), Tauramin® 12.6% (0.62 g/l) or Synthamin® 10% (0 g/l). Tauramin® 10% and Primene® 10% were packaged in glass containers whereas Tauramin® 12.6% and Synthamin® 10%, in plastic. The contents of each bag were filtered using Pall NEO96E 0.2 micron filters. A 2.25% area of each filter was observed by scanning electron microscopy at 100x magnification. The analysis by energy dispersive spectroscopy (EDS) was performed at 1,000x magnification. Results: in the Primene® 10% and Tauramin® 10% filters, a greater amount of precipitate was observed than with Tauramin® 12.6% and Synthamin® 10%. The percentage of copper and sulphur in each area of the filters studied was, respectively, 22.9% and 11.5% (Primene® 10%), 19.3% and 9.6% (Tauramin® 10%), 3.7% and 0% (Tauramin® 12.6%), 2.5% y 0% (Synthamin® 10%). Conclusions: the observed precipitate contains copper and sulphur. Precipitate formation occurs in high cysteine content amino acids solutions packaged in glass containers. It is important to use filters in the administration of PN to ensure that this type of precipitates are retained and do not pass to the patient. Key words.

Mechanism of Action and Pharmacology of Patiromer, a Nonabsorbed Cross-Linked Polymer That Lowers Serum Potassium Concentration in Patients With Hyperkalemia.

Hyperkalemia is a potentially life-threatening condition, and patients who have chronic kidney disease, who are diabetic, or who are taking renin–angiotensin–aldosterone system inhibitors are at increased risk. Therapeutic options for hyperkalemia tend to have limited effectiveness and can be associated with serious side effects. Colonic potassium secretion can increase to compensate when urinary potassium excretion decreases in patients with renal impairment, but this adaptation is insufficient and hyperkalemia still results. Patiromer is a novel, spherical, nonabsorbed polymer designed to bind and remove potassium, primarily in the colon, thereby decreasing serum potassium in patients with hyperkalemia. Patiromer has been found to decrease serum potassium in patients with hyperkalemia having chronic kidney disease who were on renin–angiotensin–aldosterone system inhibitors. Results of nonclinical studies and an early phase clinical study are reported here. Two studies with radiolabeled drug, one in rats and the other in dogs, confirmed that patiromer was not absorbed into the systemic circulation. Results of an in vitro study showed that patiromer was able to bind 8.5 to 8.8 mEq of potassium per gram of polymer at a pH similar to that found in the colon and had a much higher potassium-binding capacity compared with other resins, including polystyrene sulfonate. In a study in hyperkalemic rats, a decrease in serum potassium was observed via an increase in fecal potassium excretion. In a clinical study in healthy adult volunteers, a significant increase in fecal potassium excretion and a significant decrease in urinary potassium excretion were observed. Overall, patiromer is a high-capacity potassium binder, and the chemical and physical characteristics of patiromer may lead to good clinical efficacy, tolerability, and patient acceptance.

Use of Potassium Citrate in Restless Leg Syndrome (RLS)

It was an incidental finding that potassium citrate is significantly effective in Restless leg syndrome (RLS). While on use of potassium citrate 1080 mg equivalent to 10 mEq potassium orally once daily for the prevention of renal calculus in a patient suffering from renal colic it was incidentally observed that it significantly relieved the RLS of the patient. To evaluate the efficacy of potassium citrate in the treatment of RLS, a study was conducted on 68 patients having moderate to severe RLS. The patients were aged between 30 and 80. It was observed that 37 (54.4%) patients were completely relieved from RLS at the end of 15 days therapy and 20 (29.4%) patients were relieved after one month and 11 (16.1%) were completely relieved after 45 days therapy. Extensive methodological study is suggested to further explore the potentiality of potassium citrate in the treatment of RLS, as very few references could be searched out which are consistent with the results of the present study.

Alkali replacement raises urinary citrate excretion in patients with topiramate-induced hypocitraturia.

The aims of this study were to assess (1) the magnitude and temporality of decreased urinary citrate excretion in patients just starting topiramate and (2) the effect of alkali replacement on topiramate-induced hypocitraturia. Study 1 was a prospective, non-intervention study in which patients starting topiramate for headache remediation provided pre- and post-topiramate 24 h urine collections for measurement of urine citrate. Study 2 was a clinical comparative effectiveness study in which patients reporting to our stone clinic for kidney stones and who were treated with topiramate were prescribed alkali therapy. Pre- and post-alkali 24 h urinary citrate excretion was compared. Data for 12 and 22 patients (studies 1 and 2 respectively) were evaluated. After starting topiramate, urinary citrate excretion dropped significantly by 30 days (P = 0.016) and 62% of patients had hypocitraturia (citrate <320 mg day(-1) ). At 60 days, urine citrate was even lower than at baseline (P = 0.0032) and 86% of patients had developed hypocitraturia. After starting alkali, urine citrate increased in stone-forming patients on topiramate (198 ± 120 to 408 ± 274 mg day(-1) ; P = 0.042 for difference). 85% of patients were hypocitraturic on topiramate alone vs. 40% after adding alkali. The increase in urinary citrate was greater in patients provided ≥ 90 mEq potassium citrate. Our study is the first to provide clinical evidence that alkali therapy can raise urinary citrate excretion in patients who form kidney stones while being treated with topiramate. Clinicians should consider alkali therapy for reducing the kidney stone risk of patients benefitting from topiramate treatment for migraine headaches or other conditions.

Potassium citrate decreases urine calcium excretion in patients with hypocitraturic calcium oxalate nephrolithiasis.

Two previous studies (<10 patients each) have demonstrated that alkali therapy may reduce urine calcium excretion in patients with calcium oxalate nephrolithiasis. The hypothesized mechanisms are (1) a decrease in bone turnover due to systemic alkalinization by the medications; (2) binding of calcium by citrate in the gastrointestinal tract; (3) direct effects on TRPV5 activity in the distal tubule. We performed a retrospective review of patients on potassium citrate therapy to evaluate the effects of this medication on urinary calcium excretion. A retrospective review was performed of a metabolic stone database at a tertiary care academic hospital. Patients were identified with a history of calcium oxalate nephrolithiasis and hypocitraturia who were on potassium citrate therapy for a minimum of 3 months. 24-h urine composition was assessed prior to the initiation of potassium citrate therapy and after 3 months of therapy. Patients received 30-60 mEq potassium citrate by mouth daily. Inclusion criterion was a change in urine potassium of 20 mEq/day or greater, which suggests compliance with potassium citrate therapy. Paired t test was used to compare therapeutic effect. Twenty-two patients were evaluated. Mean age was 58.8 years (SD 14.0), mean BMI was 29.6 kg/m(2) (SD 5.9), and gender prevalence was 36.4% female:63.6% male. Mean pre-treatment 24-h urine values were as follows: citrate 280.0 mg/day, potassium 58.7 mEq/day, calcium 216.0 mg/day, pH 5.87. Potassium citrate therapy was associated with statistically significant changes in each of these parameters-citrate increased to 548.4 mg/day (p < 0.0001), potassium increased to 94.1 mEq/day (p < 0.0001), calcium decreased to 156.5 mg/day (p = 0.04), pH increased to 6.47 (p = 0.001). Urine sodium excretion was not different pre- and post-therapy (175 mEq/day pre-therapy versus 201 mEq/day post-therapy, p = NS). Urinary calcium excretion decreased by a mean of 60 mg/day on potassium citrate therapy-a nearly 30 % decrease in urine calcium excretion. These data lend support to the hypothesis that alkali therapy reduces urine calcium excretion.

Abstract 19360: Potassium Infusion at the Onset of CPR Prevents Mitochondrial Impairment After Prolonged VF Arrest

Introduction: Potassium-based cardioplegia has been used for decades in cardiac surgery to preserve cardiac tissue while inducing cardiac standstill. Recent studies have also shown that animals can be successfully resuscitated after infusion of potassium at the beginning of cardiopulmonary resuscitation (CPR). This study tested the hypothesis that infusion of potassium at the onset of CPR prevents mitochondrial impairment caused by reperfusion injury after prolonged cardiac arrest. Methods: After 15 minutes of untreated ventricular fibrillation (VF), 18 pigs were randomized to receive control saline, 50 mEq potassium (low-dose), or 100 mEq potassium (high-dose) via central venous catheter at the initiation of CPR. All animals received mechanical CPR with active compression/decompression, an impedance threshold device, and epinephrine per standard AHA protocols. Cardiac tissue was harvested after 4 minutes of CPR without defibrillation. Primary endpoints included mitochondrial respiratory control index (RCI) and mitochondrial calcium retention capacity (CRC). Secondary endpoints included the hemodynamic assessment. Results: Infusion of potassium at the onset of CPR had no effect on hemodynamics including coronary perfusion pressure (25 vs. 28, p=0.7 for Control and low-dose KCl, respectively). Despite similar hemodynamics, potassium infusion improved RCI comparing control to low-dose KCl infusion using both complex I (4.3 vs. 6.1, p=0.01) and complex II (2.4 vs. 3.3, p=0.003) substrates. High-dose KCl did not provide additional respiration benefit. Potassium infusion also increased CRC. With complex I substrates, high-dose KCl enhanced CRC compared to controls [1361 vs. 1040, (in nmol), p=0.008, respectively]. Low-dose KCl increased CRC with complex II (1337 vs. 1597, p=0.02, for control and low-dose KCl, respectively) while high-dose KCl did not provide additional benefit. Conclusions: Potassium infusion at the initiation of CPR prevents reperfusion-induced mitochondrial damage. This improvement was independent of the perfusion pressure achieved during CPR. Improvement of mitochondrial function and stability is observed within the first four minutes of CPR providing an improved substrate for establishing ROSC.

Renal potassium handling in the pregnant rat (892.13)

The fetus requires a large amount of potassium for normal development. To accommodate this need the normal pregnant rat accumulates ~6.3 mEq of potassium over the course of gestation, over 70% of which is retained during late pregnancy. However, the mechanism of potassium retention during pregnancy is largely unknown. The purpose of this study was to examine the mechanism permitting increased potassium reabsorption in the setting of high circulating aldosterone and enhanced distal nephron sodium reabsorption in the pregnant rat. Recent work on the WNK kinases has provided interesting targets for divergent modulation of sodium and potassium handling in the distal nephron. We measured the mRNA expression of WNK1, WNK3, WNK4, and ROMK in the renal cortex and outer medulla of virgin (V, n=5), mid pregnant (MP, n=5), and late pregnant (LP, n=7) rats using quantitative real‐time PCR. We found increased WNK3 expression in the outer medulla of LP rats compared to V (156 ±15 vs 100±10 % Control). The expression level of the other genes tested did not appear to differ with pregnancy state in either the cortex or the outer medulla. ROMK is the major potassium secretory channel and WNK3 is an inhibitor of ROMK activity. Therefore, the potassium retention of late pregnancy could be due in part to increased outer medullary WNK 3 expression as well as a failure of the expected aldosterone mediated transcriptional increase in ROMK.

A Case of Hypokalemia with Synthetic Cannabinoid Use

Synthetic cannabinoids cause a variety of central nervous symptoms, tachycardia and hypokalemia. We report a 27 old male patient was admitted to emergency room due to altered consciousness and vomiting. The patient declared that he smoked herbal incense named Bonzai. After a few hours he was found by his friends with impaired consciousness, no verbal response, and tonic seizure of upper extremities. He vomited once and denied intractable vomiting and diarrhea. His past medical history was nonsignificant and he was not taking any prescription drugs. Potassium (K+) and ethanol concentration was low at the time of admission (2.7 meq/l and 18 mg/dl, respectively). After infusion of 60 meq potassium chloride (KCl), repeat K+ value was 3.5 meq/l. Twenty four hours after admission K+ level dropped to 3.2 meq/l. Potassium level reached to normal value (5 meq/l) after 40 meq KCL infusion. He was discharged uneventfully. Hypokalemia due to synthetic cannabinoid usage may be due to a number of mechanisms including potassium loss via kidneys, potassium loss due to excessive sweating and diarrhea, and potassium shift into cells. Although our patient vomitted once, gastrointestinal loss may not be the sole explanation to hypokalemia. It must be kept in mind that there may be causes of hypokalemia other than vomiting in setting of synthetic cannabinoid use.

Initial large-dose administration of modified St. Thomas' solution

We introduced an initial large dose of modified St. Thomas' Hospital cardioplegic solution with the aim of providing both myocardial protection as well as a smooth intraoperative process. In 90 cases of isolated aortic valve replacement, we used the modified technique of cardioplegia in 45 (group S) and conventional administration of glucose-insulin-potassium solution in 45 (group G). The patients were selected at random. In group S, we added 4 mEq of potassium to the original St. Thomas' Hospital solution and administered 30 mL·kg(-1) as an initial dose. The temperature was decreased to 2. The mean of reperfusion time after declamping in group S was significantly shorter (16.7 ± 6.4 vs. 21.5 ± 10.0 min; p = 0.007). The average of postoperative maximum creatine kinase-MB was significantly lower in group S (25.6 ± 9.5 vs. 40.6 ± 37.2 IU·L(-1); p = 0.014). On multivariate analysis, use of the modified cardioplegia and aortic crossclamp time were significantly associated with creatine kinase-MB level and reperfusion time after declamping. This modified technique was an acceptable option that provided a bloodless operative field and avoided multiple cardioplegic administrations.

Refractory Hypokalemia, Hypomagnesemia Following Hydrochlorothiazide Use in a Patient With Inclusion Body Myositis Secondary to HTLV

Abstract INTRODUCTION: Diuretic therapy is a leading cause of hypokalemia seen in 15-50% of patients. Hypokalemia,hypomagnesemia and hypercalcemia are common with Hydrochlorthiazide use which usually resolves on stopping. Wepresent an unusual case of refractory hypokalemia, hypomagnesmia and hypophosphatesemia secondary toHydrocholorthiazide.CASE PRESENTATION: 67 Year old African American female presented to ED with altered mental status. She had historyof Inclusion Body Myositis (IBM) secondary to HTLV since 1995 and was bedbound due to muscular weakness. Medicalhistory included hypertension for which she was on Hydrochlorthiazide 25mg daily. She had presented to the ED a week agocomplaining of headache and high blood pressure of 180/99. She was treated in the ER and later discharged onHydrochlorthiazide 50mg daily. Four days later home health attendant noticed change in mentation and confusion whichprompted the ED visit. Patient was taking both Hydrochlorthiazide 25mg and 50 daily.Admission serum sodium was 106meq/l, potassium 2.7 meq/l and ionized calcium 1.04 mmol/l. Complete blood count and liver function tests were normal.She was admitted to MICU for symptomatic Hyponatremia. On therapy with hypertonic saline, her mental status improvedgradually. Admission X ray revealed bi basilar pneumonia. On the second ICU day she developed acute on chronicrespiratory failure and was intubated and mechanical ventilated. ICU course was complicated by septic shock and ARDSsecondary to aspiration pneumonia. CT chest ruled out pulmonary embolism and showed extensive bilateral lower lobe lobarinfiltrates. Patient developed thrombocytopenia and coagulopathy secondary to sepsis that resolved. By second week in ICUthere was resolution of septic shock and ARDS. She failed multiple attempt of weaning and underwent tracheostomy. Duringthe entire hospital stay she had persistent hypokalemia, hypomagnesaemia and hypocalcemia. Potassium was aggressivelyreplaced but levels remained low. Trans-tubular potassium gradient (TTKG) was 9 consistent with renal potassium wasting.Plasma renin activity was 3.1 ng/mL/h and serum aldosterone level was 1ng/dl. Her Cortisol and thyroid profile was normal.She continued to have persistent hypokalemia despite aggressive electrolyte replacement of potassium, magnesium, andcalcium daily. TTKG repeated remained high. During her hospital stay she has received a total of 2793 meq of potassium,80600 mg of magnesium and 45750 mg of calcium. Despite these replacements she continues to have low potassium andher electrolytes are monitored daily with additional replacements.DISCUSSIONS: TTKG is a useful tool in the diagnosis of hypokalemia. TTKG of > 3 generally indicate renal potassiumlosses. Renal potassium wasting related to tubular defects is seen in various conditions such as RTA, Liddles syndrome,syndrome of apparent mineralocorticoid excess, Bartter's syndrome and Gitelman's syndrome. Endocrinopathies resulting inrenal potassium wasting include Conn's syndrome, Cushing syndrome and thyrotoxicoxis. Hydrochlorthiazide can causeHyponatremia, hypokalemia, hypomagnesemia but however results in hypercalcemia. In our patient there was no evidence ofany electrolyte imbalance prior to admission which excluded the congenital syndromes. Work up for endocrinopathies wasnegative. Hydrochlorthiazide was attributed as the causal agent for refractory hypokalemia and hypomagnesemia and thehypocalcemia was attributed to Vitamin D deficiency.