Hyperkalemia in Emergency Medicine
No Results
No Results
processing….
Hyperkalemia can be difficult to diagnose clinically because symptoms may be vague or absent. The fact, however, that hyperkalemia can lead to sudden death from cardiac arrhythmias requires that physicians be quick to consider hyperkalemia in patients who are at risk for it. [17, 20] See the electrocardiogram below.
See also Can’t-Miss ECG Findings, Life-Threatening Conditions: Slideshow, a Critical Images slideshow, to help recognize the conditions shown in various tracings.
Patients with hyperkalemia may be asymptomatic, or they may report the following symptoms (cardiac and neurologic symptoms predominate):
Generalized fatigue
Weakness
Paresthesias
Paralysis
Palpitations
Evaluation of vital signs is essential for determining the patient’s hemodynamic stability and the presence of cardiac arrhythmias related to hyperkalemia. [1] Additional important components of the physical exam may include the following:
Cardiac examination may reveal extrasystoles, pauses, or bradycardia
Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength
In rare cases, muscular paralysis and hypoventilation may be observed
Signs of renal failure, such as edema, skin changes, and dialysis sites, may be present
Signs of trauma may indicate that the patient has rhabdomyolysis, which is one cause of hyperkalemia
See Clinical Presentation for more detail.
Laboratory studies
The following lab studies can be used in the diagnosis of hyperkalemia:
Potassium level: The relationship between serum potassium level and symptoms is not consistent; for example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients; the rapidity of change in the potassium level influences the symptoms observed at various potassium levels
Blood urea nitrogen (BUN) and creatinine levels: For evaluation of renal status
Calcium level: If the patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances)
Glucose level: In patients with diabetes mellitus
Digoxin level: If the patient is on a digitalis medication
Arterial or venous blood gas: If acidosis is suspected
Urinalysis: To look for evidence of glomerulonephritis if signs of renal insufficiency without a known cause are present
Cortisol and aldosterone levels: To check for mineralocorticoid deficiency when other causes are eliminated
Electrocardiography
Electrocardiography is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. Electrocardiographic changes have a sequential progression that roughly correlates with the patient’s potassium level. Potentially life-threatening arrhythmias, however, can occur without distinct electrocardiographic changes at almost any level of hyperkalemia.
See Workup for more detail.
Prehospital care
Prior to reaching the emergency department, treatment of a patient with hyperkalemia includes the following:
A patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should have intravenous access established and should be placed on a cardiac monitor [2]
In the presence of hypotension or marked QRS widening, intravenous bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate
Avoid calcium if digoxin toxicity is suspected; magnesium sulfate (2 g over 5 min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias
Inhospital care
Once the patient reaches the emergency department, assessment and treatment include the following:
Continuous ECG monitoring with frequent vital sign checks: When hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received
Assessment of the ABCs and prompt evaluation of the patient’s cardiac status with an electrocardiogram (ECG)
Discontinuation of any potassium-sparing drugs or dietary potassium
If the hyperkalemia is known to be severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause. Individualize treatment based upon the patient’s presentation, potassium level, and ECG.
Dialysis is the definitive therapy in patients with renal failure or in whom pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis, as pharmacologic therapy alone is not likely to adequately bring down the potassium levels in a timely fashion.
Medications
Drugs used in the treatment of hyperkalemia include the following:
Calcium (either gluconate or chloride): Reduces the risk of ventricular fibrillation caused by hyperkalemia
Insulin administered with glucose: Facilitates the uptake of glucose into the cell, which results in an intracellular shift of potassium
Alkalinizing agents: Increases the pH, which results in a temporary potassium shift from the extracellular to the intracellular environment; these agents enhance the effectiveness of insulin in patients with acidemia
Beta2-adrenergic agonists: Promote cellular reuptake of potassium
Diuretics: Cause potassium loss through the kidney
Binding resins: Promote the exchange of potassium for sodium in the gastrointestinal (GI) system
Magnesium sulfate: Has been successfully used to treat acute overdose of slow-release oral potassium
See Treatment and Medication for more detail.
Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose because of a paucity of distinctive signs and symptoms. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether electrocardiographic signs of electrolyte imbalance are present.
Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with the concentration gradient maintained by the sodium- and potassium-activated adenosine triphosphatase (Na+/K+ –ATPase) pump. The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential. Small changes in the extracellular potassium level can have profound effects on the function of the cardiovascular and neuromuscular systems. The normal potassium level is 3.5-5.0 mEq/L, and total body potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).
Minute-to-minute levels of potassium are controlled by intracellular to extracellular exchange, mostly by the sodium-potassium pump that is controlled by insulin and beta-2 receptors. A balance of GI intake and renal potassium excretion achieves long-term potassium balance.
Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L. [1] Ranges are as follows:
5.5-6.0 mEq/L – Mild
6.1-7.0 mEq/L – Moderate
7.0 mEq/L and greater – Severe
Hyperkalemia results from the following:
Decreased or impaired potassium excretion – As observed with acute or chronic renal failure [3] (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
Additions of potassium into extracellular space – As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)
Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) – As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)
Fictitious or pseudohyperkalemia – As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis
Hyperkalemia is diagnosed in up to 8% of hospitalized patients. A retrospective study by Betts et al estimated that in 2014, 3.7 million US adults (1.55%) had hyperkalemia, an increase over 2010. Within the adult hyperkalemic population in 2014, chronic kidney disease (CKD) and/or heart failure existed in 48.43%, with the annual prevalence of hyperkalemia in patients with CKD and/or heart failure that year being 6.35%. [19]
The male-to-female ratio is 1:1.
The primary cause of morbidity and death is potassium’s effect on cardiac function. [4, 22, 23] The mortality rate can be as high as 67% if severe hyperkalemia is not treated rapidly. [5]
A study by Krogager et al indicated that in patients who need diuretic treatment following a myocardial infarction, a potassium level above or below the 3.9-4.5 mmol/L range significantly increases the mortality risk, with the highest risk (38.3% mortality rate at 90-day follow-up) found in patients with severe hyperkalemia (>5.5 mmol/L). [6]
A study by Norring-Agerskov indicated that hyperkalemia is associated with increased 30-day mortality in hip-fracture patients, with a hazard ratio of 1.93. The study included 7293 patients with hip fracture, aged 60 years or older. [7]
Tran HA. Extreme hyperkalemia. South Med J. 2005 Jul. 98(7):729-32. [Medline].
Khanna A, White WB. The management of hyperkalemia in patients with cardiovascular disease. Am J Med. 2009 Mar. 122(3):215-21. [Medline].
Einhorn LM, Zhan M, Hsu VD, et al. The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med. 2009 Jun 22. 169(12):1156-62. [Medline].
Segura J, Ruilope LM. Hyperkalemia risk and treatment of heart failure. Heart Fail Clin. 2008 Oct. 4(4):455-64. [Medline].
Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008 Dec. 36(12):3246-51. [Medline].
Krogager ML, Eggers-Kaas L, Aasbjerg K, et al. Short-term mortality risk of serum potassium levels in acute heart failure following myocardial infarction. Eur Heart J Cardiovasc Pharmacother. 2015 Oct. 1 (4):245-251. [Medline]. [Full Text].
Norring-Agerskov D, Madsen CM, Abrahamsen B, et al. Hyperkalemia is Associated with Increased 30-Day Mortality in Hip Fracture Patients. Calcif Tissue Int. 2017 Feb 17. [Medline].
Schepkens H, Vanholder R, Billiouw JM, Lameire N. Life-threatening hyperkalemia during combined therapy with angiotensin-converting enzyme inhibitors and spironolactone: an analysis of 25 cases. Am J Med. 2001 Apr 15. 110(6):438-41. [Medline].
Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology. 1975 Jul. 43(1):89-99. [Medline]. [Full Text].
Hawkins RC. Poor knowledge and faulty thinking regarding hemolysis and potassium elevation. Clin Chem Lab Med. 2005. 43(2):216-20. [Medline].
Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective?. J Am Soc Nephrol. 2010 May. 21(5):733-5. [Medline].
Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective?. J Am Soc Nephrol. 2010 May. 21(5):733-5. [Medline].
Rogers FB, Li SC. Acute colonic necrosis associated with sodium polystyrene sulfonate (Kayexalate) enemas in a critically ill patient: case report and review of the literature. J Trauma. 2001 Aug. 51(2):395-7. [Medline].
McGowan CE, Saha S, Chu G, Resnick MB, Moss SF. Intestinal necrosis due to sodium polystyrene sulfonate (Kayexalate) in sorbitol. South Med J. 2009 May. 102(5):493-7. [Medline].
Lee J, Moffett BS. Treatment of pediatric hyperkalemia with sodium polystyrene sulfonate. Pediatr Nephrol. 2016 May 23. [Medline].
Beccari MV, Meaney CJ. Clinical utility of patiromer, sodium zirconium cyclosilicate, and sodium polystyrene sulfonate for the treatment of hyperkalemia: an evidence-based review. Core Evid. 2017. 12:11-24. [Medline]. [Full Text].
Simon LV, Farrell MW. Hyperkalemia. 2018 Jan. [Medline]. [Full Text].
Te Dorsthorst RPM, Hendrikse J, Vervoorn MT, van Weperen VYH, van der Heyden MAG. Review of case reports on hyperkalemia induced by dietary intake: not restricted to chronic kidney disease patients. Eur J Clin Nutr. 2018 Mar 27. [Medline].
Betts KA, Woolley JM, Mu F, McDonald E, Tang W, Wu EQ. The prevalence of hyperkalemia in the United States. Curr Med Res Opin. 2018 Feb 21. 1-8. [Medline].
Viera AJ, Wouk N. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2015 Sep 15. 92 (6):487-95. [Medline]. [Full Text].
Loutradis C, Tolika P, Skodra A, Avdelidou A, Sarafidis PA. Prevalence of Hyperkalemia in Diabetic and Non-Diabetic Patients with Chronic Kidney Disease: A Nested Case-Control Study. Am J Nephrol. 2015. 42 (5):351-60. [Medline].
Grodzinsky A, Goyal A, Gosch K, et al. Prevalence and Prognosis of Hyperkalemia in Patients with Acute Myocardial Infarction. Am J Med. 2016 Aug. 129 (8):858-65. [Medline]. [Full Text].
Sarwar CM, Papadimitriou L, Pitt B, et al. Hyperkalemia in Heart Failure. J Am Coll Cardiol. 2016 Oct 4. 68 (14):1575-89. [Medline]. [Full Text].
Kovesdy CP. Updates in hyperkalemia: outcomes and therapeutic strategies. Rev Endocr Metab Disord. 2017 Mar. 18 (1):41-7. [Medline]. [Full Text].
Stiles S. FDA Approves Potassium-Binder Patiromer (Veltassa), New Option for RAAS-Inhibitor–Treated Patients. Medscape. 2015 Oct 21. [Full Text].
Brown T. FDA Approves Lokelma for Hyperkalemia. Medscape Medical News. 2018 May 18. [Full Text].
David Garth, MD Attending Physician, Department of Emergency Medicine, Mary Washington Hospital
David Garth, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center
Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Hyperkalemia in Emergency Medicine
Research & References of Hyperkalemia in Emergency Medicine|A&C Accounting And Tax Services
Source
0 Comments