Retrospective Review of the Frequency of ECG Changes in Hyperkalemia

Montague, Brian T.; Ouellette, Jason R.; Buller, Gregory K.

doi:10.2215/cjn.04611007

Cited by 195 publications

(140 citation statements)

References 15 publications

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“…In addition, ventricular fibrillation may develop without preceding cardiac rhythm abnormalities, and it is difficult to predict which patients are at risk for cardiac manifestations of hyperkalemia. [33][34][35] The absolute level of serum potassium associated with an increased risk of ventricular arrhythmias and sudden cardiac death will, in part, depend on the rate of rise of serum potassium, the level of tissue potassium (as reflected by red blood cell potassium concentration), calcium concentration, pH, and other factors. These considerations support instituting acute therapy for patients with moderate-to-severe hyperkalemia according to the criteria specified above, 33 although minimal evidence from clinical trials is available on the acute treatment of hyperkalemia.…”

Section: Practical Clinical Management Of Hyperkalemia Acute Hyperkalmentioning

confidence: 99%

New Potassium Binders for the Treatment of Hyperkalemia

Pitt

Bakris

2015

Hypertension

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H yperkalemia is a clinical problem with potential mechanisms ranging from increased cellular potassium release (eg, pseudohyperkalemia, metabolic acidosis) to reduced potassium excretion (eg, reduced responsiveness to aldosterone, reduced aldosterone secretion, reduced distal sodium, and water delivery).1,2 Patients with chronic kidney disease (CKD), defined as an estimated glomerular filtration rate (eGFR) <45 mL/min per 1.73 m 2 , are at increased risk of hyperkalemia, resulting from ≥1 of these mechanisms.3 Renin-angiotensinaldosterone system inhibitors (RAASis) are recommended by guidelines for lowering blood pressure, slowing CKD progression in patients with CKD, 4,5 and reducing cardiovascular mortality and heart failure hospitalizations in patients with heart failure and a reduced ejection fraction, 6,7 but these drugs compound the hyperkalemia risk. 1,[8][9][10] The risk is magnified when the drugs are used in combination (eg, aliskiren in combination with ACE inhibitors or angiotensin receptor blockers; 8,11 mineralocorticoid receptor antagonists in combination with ACE inhibitors or angiotensin receptor blockers). Moreover, the risk for hyperkalemia is magnified in diseases, such as diabetes mellitus and heart failure. 4,5,12,13 The occurrence or fear of inducing hyperkalemia has led to premature discontinuation, suboptimal dosing, and often failure to use an RAASi, thereby exposing patients to increased cardiovascular risk.Current treatment approaches for chronic hyperkalemia are limited. Options for the management of hyperkalemia include discontinuation or reduced doses of RAASi, administration of loop diuretics, dietary potassium restriction, or sodium polystyrene sulfonate.14 None of these approaches are optimal because they require withholding life-saving or kidney preserving therapy (ie, RAASi), have a low rate of patient adherence (eg, dietary restriction), or have an unfavorable adverse effect profile and low tolerability (ie, sodium polystyrene sulfonate). 15 New agents to treat hyperkalemia are in the late stages of development. Clinical trial data suggest that these new agents effectively lower serum potassium and are well tolerated. [16][17][18][19][20] Therefore, these agents offer promising advantages over existing management options. It is possible that these agents might also facilitate maintenance of RAASi across the broad spectrum of patients with RAASi intolerance because of hyperkalemia (eg, CKD and heart failure), 18 and testing this hypothesis in larger clinical trials is warranted. This article reviews the clinical problem of hyperkalemia and identifies predictors of hyperkalemia in patients with hypertension, CKD, diabetes mellitus, and heart failure. It also presents recent clinical trial evidence of the efficacy and safety of new treatments for hyperkalemia, and it discusses how these agents may be used clinically, if approved. Overview of HyperkalemiaThe rate of hyperkalemia is low in uncomplicated hypertension patients treated with RAASi, 21 but it rises in the setting o...

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Section: Practical Clinical Management Of Hyperkalemia Acute Hyperkalmentioning

confidence: 99%

New Potassium Binders for the Treatment of Hyperkalemia

Pitt

Bakris

2015

Hypertension

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“…Hyperkalemia induced flaccid paralysis has been described mostly in the setting of end-stage renal disease, typically affecting lower extremities, and sometimes associated with ascending paralysis, but also focal neurological deficits have been described [4]. Shortening of the QT interval and peaked T waves (Figures 3 and 4), as well as other typical ECG changes are often observed in these patients [5][6][7]. If treatment for hyperkalemia is instituted promptly, complete recovery of the hyperkalemia-induced tetraplegia is achieved in 89% of patients [8].…”

Section: Case Presentationmentioning

confidence: 99%

Acute Reversible Tetraplegia Induced by Hyperkalemia in a Patient with Paravertebral Mass due to Lymphoma

Tinoco¹,

Kanji²,

Hosein³

2013

J Clin Case Rep

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Acute onset of tetraplegia is a medical emergency. Hyperkalemia has been described as a very uncommon cause of tetraplegia. A 79 year old male presented with an acute onset of tetraplegia. His past medical history was significant for stage III follicular lymphoma diagnosed 4 years ago that 1 month prior to the admission progressed with biopsy-proven transformation to a diffuse large B-cell lymphoma. Recent CT and PET scans revealed multiple active lesions including a large paravertebral mass measuring 29 cm×12 cm×7 cm starting in the axial level of the diaphragm involving left psoas, the left renal vein and encasing the aorta. Multiple skeletal lesions, as well as numerous lymph nodes were found. The liver and spleen were also compromised. His surgical history was remarkable for radical prostatectomy for localized prostate cancer. The patient did not have previous history of renal failure and his blood urea nitrogen and creatinine were within normal range (15 mg/dL and 0.8 mg/dL, respectively). Case PresentationTwo days prior to presentation, the patient began experiencing malaise, weakness and myalgia in his lower extremities, which progressed to paraparesis several hours later, and he was unable to ambulate without assistance. Thereafter he developed weakness in both upper extremities. On the day of admission he suddenly became completely tetraplegic. He denied seizures, chorea, rigidity, spasms, recent trauma, or any recent febrile or viral illness. He did admit to have experienced recent poor oral intake related to his generalized malaise, with no vomiting or diarrhoea and he denied recent use of non-steroidal anti-inflammatory drugs or any other new medications, including steroids).On admission his vital signs were all within normal limits; the blood pressure was 136/76 mmHg, heart rate was 68 per minute, respiratory rate was 18 per minute, and temperature was 36.6 degrees Celsius. He was alert and oriented, in no distress with flaccid tetraplegia, areflexia, preserved cranial nerve function, normal rectal sphincter tone and absent plantar responses. The electrocardiogram showed wide QRS complexes, a shortened QT interval and tall peaked T waves. Laboratory testing revealed a serum potassium of 9.3 mEq/L, sodium 120 mEq/L, urea nitrogen 81 mg/dL, creatinine 9.9 mg/dL, calcium 8.5 mg/dL, phosphorus 4.1 mEq/L, creatine kinase 126 units/L, uric acid 9.6 mg/ dl, Lactate Dehydrogenase (LDH) 1118 mg/dl (LDH was 1114, two weeks earlier), aspartate transaminase 28 IU/L, alanine transaminiase 23 IU/L, and alkaline phosphatase 65 IU/L. Imaging studies were negative for hydronephrosis and there was no evidence of spinal cord involvement on chest, abdominal and pelvic CTs performed only two weeks before the admission.While spinal cord compression was considered in the differential diagnosis, however hyperkalemia induced flaccid paralysis with severe acute renal failure were more likely causes and the decision was to initiate treatment of hyperkalemia and renal failure before proceeding with dedicated studies to...

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“…abnormalities have a poor sensitivity and specificity for identifying hyperkalaemia in stable patients (Montague, 2008). This is something recognized by Barash et al (2009), who state that the ECG should provide a suggestion of hyperkalaemia but that the focus be upon the medical history (with emphasis on drug history) and assessment of renal function.…”

Section: H E a L T H C A R Ementioning

confidence: 99%

“…Unfortunately, there is no widely excepted definition of a peaked T wave, but some have suggested envisaging it as a seat-if it is too uncomfortable to sit on, then it is likely to be peaked (Toy et al, 2009 (Montague, 2008). This is something recognized by Barash et al (2009), who state that the ECG should provide a suggestion of hyperkalaemia but that the focus be upon the medical history (with emphasis on drug history) and assessment of renal function.…”

Section: The Ecgmentioning

confidence: 99%

Prehospital treatment of hyperkalaemia

Strange

2010

Journal of Paramedic Practice

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This article explores the assessment and management considerations of patients with hyperkalaemia. Using a case study from clinical practice, the hospital treatment is reviewed with particular emphasis upon the use of calcium, insulin and dextrose. In particular, potential prehospital treatments are considered, with focus upon the use of salbutamol and furosemide. Definitions, incidence and mortality rates of hyperkalaemia are also detailed. The signs, symptoms and causes of the condition are examined, with the aim of achieving prehospital diagnosis in the absence of serum potassium levels. Hyperkalaemic electrocardiogram (ECG) changes are studied and examples are given. Conclusions are made, including a recommendation for the prehospital use of salbutamol in the treatment of hyperkalaemia. (Khedr et al, 2009). A clear understanding of the emergency management is crucial as hyperkalaemia has lethal consequences and is associated with a mortality rate of 14-41% (Feld and Kaskel, 2010). Furthermore, severe hyperkalaemia, if not treated rapidly, carries a mortality rate of 67% (Weisberg, 2008), providing a compelling argument for treating the condition in the prehospital phase. Key wordsl Diagnosis Signs and symptomsTo carry out appropriate management of hyperkalaemic patients, an understanding of the signs and symptoms is fundamental. An increased concentration of potassium in the plasma has the effect of depolarizing cell membranes, therefore making them less excitable and in turn, resulting in neuromuscular dysfunction (Lubin et al, 2006). Patients with hyperkalaemia can display abnormal signs and symptoms specific to the renal, gastrointestinal, cardiovascular and nervous systems (LeFever Kee et al, 2009). They can present with nausea, abdominal pain and or/diarrhoea (Guy, 2009); but also muscle irritability, malaise, muscle weakness and, in patients with serum potassium levels of greater than 6.0 mEq/L, paresthesia and an increased heart rate (LeFever Kee et al, 2009).Despite such an array of symptoms, it is commonly documented that, even with severe hyperkalaemia, patients can present with no abnormalities (Gleadle, 2007;Baltazar, 2009). This would explain Mrs Y's asymptomatic presentation, making diagnosing the condition in the prehospital environment difficult, if not impossible. BloodsIn Mrs Y's case, the diagnosis had been made on the basis of blood results and a history of reduced renal function-a well recognized cause of hyperkalaemia (Irwin and Rippe, 2008). In the presence of normal renal function, the attending doctor would suspect 'pseudohyperkalaemia', a condition in which abnormal potassium levels are the result of haemolysis in-vitro (Irwin and Rippe, 2008). However, such factors are not of concern to UK paramedics as, despite evidence-based approval (Prause et al, 1997), blood gas and electrolyte testing is currently unavailable in the prehospital stage. The ECGWithout the help of serum potassium results and without the benefit of specific signs and symptoms, diagnosing hyperkalaemia in...

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Retrospective Review of the Frequency of ECG Changes in Hyperkalemia

Cited by 195 publications

References 15 publications

New Potassium Binders for the Treatment of Hyperkalemia

New Potassium Binders for the Treatment of Hyperkalemia

Acute Reversible Tetraplegia Induced by Hyperkalemia in a Patient with Paravertebral Mass due to Lymphoma

Prehospital treatment of hyperkalaemia

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