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• W2912351704 abstract "A 66-year-old white man with a medical history of chronic kidney disease (CKD) stage 3a (baseline creatinine level of 1.4 mg/dL; normal 0.74-1.35 mg/dL) with an estimated glomerular filtration rate of 52 mL/min per 1.73 m2 per the Chronic Kidney Disease Epidemiology collaboration equation, controlled type 2 diabetes mellitus with microalbuminuria, hypertension, hyperlipidemia, and medically complicated obesity (body mass index, 37) presented to his primary care clinic with episodes of orthostatic light-headedness that had been occurring for approximately 2 weeks. These episodes were also associated with chest tightness and dyspnea. Symptoms occurred only while standing or ambulating and never while at rest. He reported no palpitations, vertiginous symptoms, recent fevers or chills, hemoptysis, known sick contacts, or insect bite exposures. His light-headedness, chest pain, and dyspnea worsened on the day before presentation, prompting a visit to his physician for further evaluation. He reported that he had been taking his blood pressure medications including amlodipine, lisinopril, atenolol, and spironolactone-hydrochlorothiazide, as well as his other medications (metformin, aspirin, and pravastatin) regularly and as instructed. He had noted a considerable decrease in his urine output over the previous day. He had no recent travel, surgical procedures, immobilization, history of pulmonary embolism (PE), deep venous thrombosis, or active malignancy. On physical examination, he appeared nontoxic but had bradycardia (heart rate, 25 beats/min) with hypotension (blood pressure, 90/40 mm Hg) and a respiratory rate of 14 breaths/min. No rashes, lymphadenopathy, or peripheral edema were noted. Heart examination revealed no murmurs, and lung examination findings were normal. He was alert and in no distress. Results of abdominal examination and the remainder of the neurologic examination were unremarkable. Given his severe symptomatic bradycardia and borderline hypotension, he was referred to the emergency department (ED) for further evaluation.1.Based on this patient’s history and physical examination findings, which one of the following diagnoses is of highest initial concern?a.PEb.Myocarditisc.Acute coronary syndrome (ACS)d.Atenolol overdosee.Hyperkalemia Although PE can lead to hypotension, as well as symptoms of dyspnea and chest discomfort, this diagnosis is less likely in the absence of tachycardia, tachypnea, or clinical signs or symptoms of deep venous thrombosis. Using the Wells criteria to determine this patient’s risk for PE revealed a score of 0, placing him in the low-risk group (1.3% chance of PE in one ED population1Wolf S.J. McCubbin T.R. Feldhaus K.M. Faragher J.P. Adcock D.M. Prospective validation of Wells Criteria in the evaluation of patients with suspected pulmonary embolism.Ann Emerg Med. 2004; 44: 503-510Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar). Myocarditis may also present very nonspecifically, including with symptoms of chest pain, palpitations, or transient electrocardiographic (ECG) changes; however, it is vital to rule out coronary artery disease and ACS that may also explain this clinical presentation.2Caforio A.L. Pankuweit S. Arbustini E. et al.Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases.Eur Heart J. 2013; 34 (2648a-2648d): 2636-2648Crossref PubMed Scopus (1820) Google Scholar In this patient’s case, even in the absence of ST-segment changes, his history of diabetes, hypertension, hyperlipidemia, and CKD increase his risk for coronary artery disease as a potential cause of his symptoms. Bradycardia may also be a presentation of infarct to the sinoatrial region of the myocardium.3Trappe H.J. Tachyarrhythmias, bradyarrhythmias and acute coronary syndromes.J Emerg Trauma Shock. 2010; 3: 137-142Google Scholar Therefore, it is essential to obtain cardiac biomarkers to further investigate. Atenolol overdose and hyperkalemia are also both plausible etiologies because of the patient’s bradycardia; but again, ACS must be considered and ruled out in this high-risk patient. In the ED, ECG revealed junctional bradycardia with loss of P waves, normal QRS complex, and peaked T waves. Laboratory evaluation yielded the following results (reference ranges provided parenthetically): hemoglobin, 11.9 g/dL (13.2-16.6 g/dL); leukocytes, 9.6 × 109/L (3.4-9.6 × 109/L); platelets, 168 × 109/L (135-317 × 109/L); sodium, 134 mmol/L (135-145 mmol/L); potassium, 7.7 mmol/L (3.6-5.2 mmol/L); creatinine, 2.4 mg/dL (0.84-1.21 mg/dL); bicarbonate, 17 mmol/L (22-29 mmol/L); glucose, 174 mg/dL (70-140 mg/dL); anion gap 13 (7-15); magnesium, 1.8 mg/dL (1.7-2.3 mg/dL); and initial troponin T, <0.01 ng/L (≤15 ng/L). Six-hour serial troponin T measurements were all <0.01 ng/L. The patient denied any intentional or unintentional overdose of atenolol.2.Which one of the following is the best treatment for the patient at this time?a.Intravenous (IV) insulinb.Inhaled β-agonistc.Sodium bicarbonated.IV normal salinee.IV calcium gluconate Intravenous insulin, either provided in bolus or through continuous infusion with IV glucose, may be used to temporarily drive potassium into the cells through intracellular shift. However, it would be a secondary treatment because it does not protect the patient from the most life-threatening outcome of persistent hyperkalemia, arrhythmia. Inhaled or IV β-agonist therapy also reduces potassium levels via intracellular shift, although up to one-third of all patients do not respond.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar The high doses used may additionally result in adverse effects such as tachycardia, anxiety, and tremors. Intravenous sodium bicarbonate may have some variable benefit in patients with metabolic acidosis undergoing hemodialysis but has failed to provide substantial or predictable reduction in other experimental populations.5Kim H.J. Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalemia in end-stage renal disease patients.Nephron. 1996; 72: 476-482Crossref PubMed Scopus (74) Google Scholar Normal saline administered IV will help to dilute potassium concentration but, much like the aforementioned treatments, does not protect from arrhythmias. Calcium salt infusion is the first step in the emergency management of hyperkalemia. Although this treatment does not affect the serum potassium concentration, it is essential in stabilizing the cardiac myocyte membranes if any ECG changes are present in the setting of hyperkalemia. It may also be beneficial in patients who do not have ECG changes but are at a higher risk of development of arrhythmia because of other electrolyte derangements or a rapidly increasing potassium level.6Kovesdy C.P. Management of hyperkalemia: an update for the internist.Am J Med. 2015; 128: 1281-1287Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Precaution should be taken with IV calcium infusion because it can lead to severe soft tissue injury or necrosis with extravasation. Our patient’s hyperkalemia was thought to be multifactorial due to a combination of his underlying medical conditions and multiple medications. He was given IV calcium gluconate in the ED and was quickly transferred to the coronary care unit, where IV insulin, inhaled β-agonists, and IV hydration were promptly administered, initially with normal saline before being transitioned to isotonic bicarbonate. Many of his home medications were withheld in the meantime. His potassium level subsequently decreased to 6.3 mmol/L. Repeated ECG revealed marked improvement in the bradycardia, but peaked T waves were still present. Blood pressure (114/45 mm Hg) and urinary output had also improved considerably with the administration of fluids.3.Which one of the following is the most appropriate intervention to decrease the patient’s total potassium level?a.IV loop diureticb.IV thiazide diureticc.Sodium polystyrene sulfonated.Hemodialysise.Patiromer In this patient with adequate urinary output and adequate hydration, the IV administration of a loop diuretic, such as furosemide, provides a rapid onset of action for the treatment of hyperkalemia, especially when compared to the other options listed. However, this intervention would not be appropriate in the setting of dehydration or for patients who do not make urine and are dependent on hemodialysis. In the setting of this patient’s acute kidney injury (creatinine clearance, <30 mL/min per 1.73 cm2 [77-160 mL/min per 1.73 cm2), thiazide diuretics are less effective than loop diuretics and the loop diuretics are preferred. Sodium polystyrene sulfonate, a cation exchange resin, has been widely used previously for the treatment of hyperkalemia, but it has fallen out of favor of late because of its erratic absorption, delayed and marginal effects, and well-described rare complication of colonic necrosis.7Hagan A.E. Farrington C.A. Wall G.C. Belz M.M. Sodium polystyrene sulfonate for the treatment of acute hyperkalemia: a retrospective study.Clin Nephrol. 2016; 85: 38-43Crossref PubMed Scopus (29) Google Scholar Therefore, this medication is not the most appropriate choice. Hemodialysis is indicated in patients with hyperkalemic emergency who have appropriate vascular access and severe renal impairment and are refractory to medical therapy. Hemodialysis has the ability to rapidly decrease serum potassium, at the rate of 1.0 to 1.5 mEq/L for each hour of dialysis.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar However, dialysis was not the optimal first treatment in this patient’s case because he was still making urine. Patiromer is a newer medication, a nonabsorbable organic polymer that binds potassium in the gastrointestinal tract and prevents its absorption. Unfortunately, it also has a delayed onset of action and would not be the most appropriate medication for this setting. Intravenous furosemide was promptly initiated in addition to the previously mentioned IV hydration. His potassium level decreased to 5.5 mmol/L in less than 12 hours. His urinary output improved further, and his light-headedness, chest tightness, and nausea completely abated. Repeated ECG revealed normal sinus rhythm.4.Which one of this patient’s known medical comorbidities played the largest role in the development of acute hyperkalemia?a.CKD with acute kidney injuryb.Medically complicated obesityc.Hypertensiond.Type 2 diabetes mellituse.Hyperlipidemia Although there were many factors that contributed to this patient’s hyperkalemia, it was likely CKD that was the most important contributor. The kidneys are responsible for excreting 90% of the body’s absorbed potassium under normal conditions, with the remainder leaving the body through the gastrointestinal tract.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar Therefore, patients with underlying CKD are at the highest risk of altered potassium homeostasis. This effect is thought to be related primarily to toxic effects to the sodium/potassium adenosine triphosphatase pump; low renin levels, and therefore low aldosterone concentrations, may also be implicated. Patients with CKD therefore have a reduced ability to excrete an acute potassium load and will have a more sustained increase in potassium in these situations.8Gennari F.J. Segal A.S. Hyperkalemia: an adaptive response in chronic renal insufficiency.Kidney Int. 2002; 62: 1-9Abstract Full Text Full Text PDF PubMed Scopus (95) Google Scholar Obesity has no major effects on potassium clearance, and hypertension may in fact be protective against hyperkalemia if left uncontrolled because aldosterone effects result in potassium loss due to effects on the epithelial sodium channel located in the collecting duct of the renal tubule. Type 2 diabetes mellitus may predispose individuals to hyperkalemia in various ways, including increased glucagon concentrations, hyperosmolality, insulin resistance, and the use of potassium-sparing medications.9Sousa A.G. Cabral J.V. El-Feghaly W.B. de Sousa L.S. Nunes A.B. Hyporeninemic hypoaldosteronism and diabetes mellitus: pathophysiology assumptions, clinical aspects and implications for management.World J Diabetes. 2016; 7: 101-111Google Scholar It is also known to be associated with an increased propensity for type 4 renal tubular acidosis (hyporeninemic hypoaldosteronism), although typically only in the presence of underlying CKD. Similar to obesity, hyperlipidemia has no major effects on potassium clearance. The patient’s hyperkalemia completely resolved after 24 hours. He was transferred to the general care ward with a plan to discharge in the following days.5.Which one of the following medications is the most important to discontinue to reduce this patient’s risk of recurrent hyperkalemia?a.Lisinoprilb.Spironolactonec.Amlodipined.Pravastatine.Atenolol Drug-induced hyperkalemia is an essential consideration in clinical practice because a variety of commonly used medications lead to alterations in potassium homeostasis. Drugs used to disrupt the renin-angiotensin-aldosterone system (RAAS), such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and aldosterone receptor blockers, are the most common culprits of drug-induced hyperkalemia; therefore, the benefits of their use must be carefully weighed with this and other risks. The ACE inhibitors act by blocking the conversion of angiotensin I to angiotensin II, resulting in reduced vasoconstriction and decreased aldosterone production. It is mainly by inducing hypoaldosteronism that they increase serum potassium levels, with hyperkalemia occurring in approximately 1.3% of low-risk patients.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar Despite this known association, data suggest that ACE inhibitors improve survival in those with non–dialysis-dependent CKD, as well as those with type 2 diabetes mellitus and hypertension; therefore, this patient’s lisinopril should be prioritized as an ongoing medication once his acute kidney injury has resolved.10Molnar M.Z. Kalantar-Zadeh K. Lott E.H. et al.Angiotensin-converting enzyme inhibitor, angiotensin receptor blocker use, and mortality in patients with chronic kidney disease.J Am Coll Cardiol. 2014; 63: 650-658Crossref PubMed Scopus (120) Google Scholar, 11van Vark L.C. Bertrand M. Akkerhuis K.M. et al.Angiotensin-converting enzyme inhibitors reduce mortality in hypertension: a meta-analysis of randomized clinical trials of renin-angiotensin-aldosterone system inhibitors involving 158,998 patients.Eur Heart J. 2012; 33: 2088-2097Crossref PubMed Scopus (346) Google Scholar, 12Eurich D.T. Majumdar S.R. Tsuyuki R.T. Johnson J.A. Reduced mortality associated with the use of ACE inhibitors in patients with type 2 diabetes.Diabetes Care. 2004; 27: 1330-1334Crossref PubMed Scopus (61) Google Scholar Spironolactone, a mineralocorticoid receptor antagonist that also has estrogenic and antiandrogenic activity, is used for a variety of indications. In this patient, the medication was used only for uncontrolled hypertension, rather than for a history of heart failure. Although the RALES (Randomized Aldactone Evaluation Study) trial suggested a decrease in all-cause mortality in patients with New York Heart Association class IV heart failure associated with the use of spironolactone, there is no known survival benefit for patients using this medication for CKD or hypertension alone.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar Additionally, the incidence of hyperkalemia increases when RAAS inhibitors are used in combination. Therefore, in this patient with CKD and a high risk for hyperkalemia, discontinuing spironolactone would likely yield the most benefit in reducing risk for future hyperkalemic events. There are no known major clinical hyperkalemic adverse effects associated with amlodipine or pravastatin. β-Blockers have been associated with hyperkalemia, especially in those with impaired renal function; however, this effect is less common with the cardioselective agents such as atenolol. The patient’s acute kidney injury resolved with ongoing rehydration. His atenolol and spironolactone were discontinued indefinitely. His lisinopril was with held for the short term, with a plan to reinitiate this medication at a reduced dose because of its well-known benefits. He was discharged home after 5 days in the hospital. Hyperkalemia is a common metabolic derangement, occurring in approximately 3.2% in the general population. In patients with CKD, incidence may reach 73% depending on the studied population.6Kovesdy C.P. Management of hyperkalemia: an update for the internist.Am J Med. 2015; 128: 1281-1287Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Because hyperkalemia can be rapid in onset, symptomatically silent, and lead to life-threatening dysrhythmias, its efficient diagnosis and treatment are essential. Although some patients may present with nonspecific symptoms such as weakness, paresthesias, nausea, or even paralysis, in many cases ECG findings may provide the first clinical evidence, especially in severe hyperkalemia. With mild potassium elevations (5.5-6.5 mmol/L), possible ECG findings include peaking of the T wave and prolongation of the PR segment. With moderate elevations (6.5-8.0 mmol/L), the P wave may be lost, with prolongation of the QRS complex and ST-segment elevations also potentially seen. With more severe hyperkalemia (>8.0 mmol/L), the QRS complex will progressively widen to sine wave morphology, with increased risk for ventricular fibrillation, severe bradycardia, or asystole.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar There is no universal guideline for the first-line treatment of hyperkalemia or at which serum potassium level therapy should be administered. Instead, treatment should be directed to the patient presentation and the acuity of electrolyte disturbance. In the presence of ECG changes, stabilization of the cardiac membrane with a calcium salt infusion is the first step in management.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar The next steps often involve intracellular shifting of potassium into the cells with insulin or inhaled β-agonists, followed by definitive treatments focused on elimination of potassium. Hyperkalemia is also a clinically important adverse effect of many medications, with medications affecting the RAAS being the most common culprits. However, β-blockers, nonsteroidal anti-inflammatory drugs, and heparin may also increase serum potassium by various mechanisms.4Sood M.M. Sood A.R. Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia.Mayo Clin Proc. 2007; 82: 1553-1561PubMed Scopus (5) Google Scholar Care should be taken in the choice of antihypertensive agent in this population, especially in those patients with underlying CKD; the focus should be on continuing medications with survival benefit while mitigating other causes of hyperkalemia such as high dietary intake, metabolic acidosis, or the use of potassium supplementation. The addition of a loop diuretic to the antihypertensive regimen may also be an appropriate option for some patients, and sodium bicarbonate may also be considered to manage metabolic acidosis in those with CKD. Additionally, limiting the intake of high-potassium foods such as bananas, melons, some citrus, dried fruits, avocados, squash, leafy greens, cruciferous vegetables, dairy products, bran, and salt substitutes may be helpful. However, emphasis should also be placed on consuming a variety of foods in smaller quantities and draining canned foods prior to preparing and serving to minimize incidental potassium intake. Novel potassium-binding agents have recently been studied for the management of hyperkalemia, patiromer and sodium zirconium cyclosilicate. Patiromer, which binds potassium in the gastrointestinal tract in exchange for sodium, was first approved by the US Food and Drug Administration for use in the treatment of hyperkalemia in 2015. It has been associated with a decreased incidence of hyperkalemia in patients with heart failure starting an aldosterone antagonist and in a more recent clinical trial was shown to decrease serum potassium levels in patients with CKD receiving RAAS inhibitor therapy.6Kovesdy C.P. Management of hyperkalemia: an update for the internist.Am J Med. 2015; 128: 1281-1287Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Sodium zirconium cyclosilicate is a nonabsorbable cation compound that exchanges sodium and hydrogen ions for potassium in the intestine. Although not yet available, randomized, placebo-controlled trials have suggested that it results in significant reductions in serum potassium levels and maintenance of normokalemia.6Kovesdy C.P. Management of hyperkalemia: an update for the internist.Am J Med. 2015; 128: 1281-1287Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar Pending further study and review, both of these medications may offer promising alternatives to sodium polystyrene sulfonate in the treatment of both chronic and acute hyperkalemia and improving tolerability of medications that have been shown to provide survival benefits." @default.
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• W2912351704 title "66-Year-Old Man With Light-headedness, Chest Pain, and Dyspnea" @default.
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