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CASE REPORT
Year : 2013  |  Volume : 40  |  Issue : 3  |  Page : 166-168

An unseen 'face' of hyperkalemia


1 Department of Internal Medicine/Critical Care, Princess Durru-Shehvar Children's and General Hospital, Purani Haveli, Hyderabad, Andhra Pradesh, India
2 Department of Internal Medicine, Princess Durru-Shehvar Children's and General Hospital, Purani Haveli, Hyderabad, Andhra Pradesh, India

Date of Web Publication19-Oct-2013

Correspondence Address:
Dilip Gude
Department of Internal Medicine/Critical Care, Princess Durru-Shehvar Children's and General Hospital, Purani Haveli, Hyderabad - 500 001, Andhra Pradesh
India
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Source of Support: Medwin Hospital, Nampally, Hyderabad, Andra Pradesh, India, Conflict of Interest: None


DOI: 10.4103/0974-5009.120051

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  Abstract 

Hyperkalemia with normal or minimal electrocardiogram (ECG) changes is not commonly encountered. The 'milder' presentation may mask and hence lead to an under-management of a severe hyperkalemia. We discuss a case of severe hyperkalemia secondary to tumor lysis syndrome and its 'innocuous' ECG changes.

Keywords: Electrocardiogram changes, hyperkalemia, tumor lysis


How to cite this article:
Gude D, Abbas A. An unseen 'face' of hyperkalemia. J Sci Soc 2013;40:166-8

How to cite this URL:
Gude D, Abbas A. An unseen 'face' of hyperkalemia. J Sci Soc [serial online] 2013 [cited 2019 May 23];40:166-8. Available from: http://www.jscisociety.com/text.asp?2013/40/3/166/120051


  Introduction Top


Hyperkalemia resulting in the typical electrocardiogram (ECG) changes reckons clinicians' attention and may be managed promptly. But cases with severe underlying hyperkalemia with minimal/absent ECG changes may undermine the severity of the case and may result in inadequate management. Very few cases have been reported worldwide with such presentation. We share our experience with one such a case and review the pertinent literature.


  Case Report Top


A 54-year-old non-diabetic and non-hypertensive woman, diagnosed with ovarian mucinous cystadenocarcinoma (and received chemotherapy a month ago), presented with gradually worsening abdominal discomfort for 20 days. On examination her blood pressure was 80 mm of Hg (systolic). Her abdomen was distended, non-tender without any guarding/rigidity and shifting dullness was positive. ECG was unremarkable except for poor progression of R wave, small voltage configuration, and inverted P waves in lead III [Figure 1]. Intravenous fluids and later inotropic support were administered and blood pressure improved eventually to 110/70 mm of Hg. Labs showed serum K+ to be 7.4 meq/L, Na+-133 meq/L, Cl-102, Hb-11g/dl, total white blood cell count (TWBC)-9500/mm 3 , Serum creatinine 2.3 mg/dl, urea 81 mg/dl, Cancer Antigen(CA)-125-1955 U/mL. Echocardiogram was unremarkable with normal left ventricular function (ejection fraction of 68%). Abdominal ultrasound showed normal-sized kidneys with decreased corticomedullary differentiation. Mild to moderate ascites was noted apart from fatty liver. Arterial blood gas analysis showed metabolic acidosis with HCO3 of 12 meq/L and pH of 7.1 and no hypoxia. Serum Calcium was 7.8 mg/dl; Serum lactate Dehydrogenase (LDH) was 1350 U/L, serum uric acid was 9.8 mg/dl, and serum phosphate 6.2 mg/dl. Computerized tomography of abdomen showed bilateral increased size of parailiac and inguinal lymph nodes with omental thickening, fat stranding, and moderate ascites. Adequate hydration, allopurinol 300 mg twice-a-day, and rasburicase 6 mg per day were added. Serum potassium over the next 4 days was 7.9, 7.4, and 7.8 despite aggressive treatment with beta-2 agonist nebulization, insulin dextrose administration, and potassium binding resins (along with calcium gluconate 30 mL only on day 1). The patient then underwent hemodialysis which resulted in a potassium level of 5.2 meq/L (after 3 sessions). The patient was then discharged with advice of close follow-up.
Figure 1: Electrocardiogram of the patient conspicuous of the absence of changes of hyperkalemia

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  Discussion Top


Our case stands out for the unusual aspect of absence of the usual changes of hyperkalemia in ECG. Normally, while the milder changes include tall peaked T waves and flattening of P waves, increasing potassium values result in loss of P waves, progressive lengthening of the PR interval and QRS widening, and nodal rhythm. More severe changes with worsening hyperkalemia result in bizarrely wide QRS, sine wave, ventricular fibrillation, and asystole. None of the above described changes were noted in our patient. A report of seven hyperkalemia cases with minimal ECG changes was noted in literature that emphasizes that absence of typical ECG changes does not preclude severe hyperkalemia. [1] A case of severe hyperkalemia in disseminated candida sepsis was reported in literature which also had a similar refractoriness to conservative hyperkalemia management. The case also sported minimal to absent ECG changes. [2]

Apart from cardiac conduction abnormalities, our patient had a conspicuous absence of muscle weakness or paralysis/paresis. Tumor-lysis syndrome (TLS) with the resultant acidosis was the main culprit for hyperkalemia in our patient. Pseudo-hyperkalemia secondary to thrombocytosis, leukocytosis, in vitro hemolysis, tight tourniquet etc., and other causes of inadequate potassium excretion such as renin-aldosterone-angiotensin system inhibition were excluded in our case. Decreased distal delivery (as in heart failure/volume depletion) and hyporeninemic hypoaldosteronism were ruled out as well. Absence of any connective tissue disorders, end-stage renal failure, and primary adrenal insufficiency further pin-pointed the etiology of hyperkalemia to TLS. TLS is an important differential diagnosis that clinicians should consider in hyperkalemia that is poorly responsive to conservative management. Our patient qualified the laboratory and clinical Cairo Bishop Criteria for TLS. Apart from persistent hyperkalemia (the major factor in our case), severe oliguria or anuria and/or hyperphosphatemia-induced symptomatic hypocalcemia are also indications for renal replacement in TLS.

Although it is widely believed that calcium gluconate need not be given in hyperkalemia in the absence of the typical ECG changes, we went ahead with its administration on the 1 st day as there were no clear-cut guidelines as to which ECG changes exactly are to be taken in to account. This is an area that demands further research and universal recommendations.

It is known that in settings of renal failure (as in our case) ECG changes typical of hyperkalemia may not manifest until serum potassium concentration exceeded 7.6 meq/L. Especially, patients on hemodialysis with hyperkalemia may not exhibit the usual ECG sequelae of hyperkalemia, probably owing to fluctuations in serum calcium concentration. [3]

Some of the atypical or nonspecific ECG changes in hyperkalemia include arrhythmias, ST changes (depression or elevation), decrease in height of R wave with development of deep S waves, QRS axis shift to the right or left, bundle branch blocks, and sino-atrial exit blocks. [4] Of the above, decrease in the height of R and left axis deviation are the only changes noted in our patient. Left ventricular hypertrophy and intraventricular conduction defects may mask the expected ECG changes. Coexistent factors such as acidosis, hypoxia, hyponatremia, and hypocalcemia augment the ECG changes via increasing myocardial sensitivity to hyperkalemia whereas hypernatremia or hypercalcemia (not seen in our case) may dampen such effects. [1] Rate of rise in potassium also may play a role in ECG manifestations (rapid rise may manifest early typical changes while delayed rise may reflect attenuated changes). [5] Our case might have had a delayed rise in potassium which could in part explain the absence of characteristic ECG changes. Another retrospective study concluded that ECG changes of hyperkalemia have low sensitivity and specificity and should not be used to guide the management. [6]


  Conclusion Top


Our case highlights that typical ECG changes might not always accompany hyperkalemia and one should not let the atypical changes undermine the severity of hyperkalemia. We also underline an important cause of refractory hyperkalemia, tumor lysis syndrome that clinicians should have a high index of suspicion of when dealing with such situations.


  Acknowledgment Top


We thank our colleagues and staff of Internal medicine.

 
  References Top

1.Martinez-Vea A, Bardají A, Garcia C, Oliver JA. Severe hyperkalemia with minimal electrocardiographic manifestations: A report of seven cases. J Electrocardiol 1999;32:45-9.  Back to cited text no. 1
    
2.Sharma S, Gupta H, Ghosh M, Padmanabhan A. Severe hyperkalemia with normal electrocardiogram. Indian J Crit Care Med 2007;11:215-7.  Back to cited text no. 2
  Medknow Journal  
3.Aslam S, Friedman EA, Ifudu O. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients. Nephrol Dial Transplant 2002;17:1639-42.  Back to cited text no. 3
    
4.Yu AS. Atypical electrocardiographic changes in severe hyperkalemia. Am J Cardiol 1996;77:906-8.  Back to cited text no. 4
    
5.Gogas BD, Iliodromitis EK, Leftheriotis DI, Flevari PG, Rallidis LS, Kremastinos DT. Instantaneous electrocardiographic changes and transient sinus rhythm restoration in severe hyperkalaemia. Int J Cardiol 2011;148:e40-2.  Back to cited text no. 5
    
6.Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008;3:324-30.  Back to cited text no. 6
    


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  In this article
Abstract
Introduction
Case Report
Discussion
Conclusion
Acknowledgment
References
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