Intradialysis Cardiac Arrest in a 40 year old Woman with Diabetic Nephropathy Precipitated by Hyperkalemia Induced by Type 4 Renal Tubular Acidosis.
DOI:
https://doi.org/10.47941/ijhs.1018Keywords:
hyperkalemia, type 4 renal tubular acidosis, metabolic acidosis, intradialysis cardiac arrest, diabetic nephropathyAbstract
Purpose: We present a rare case of intra-dialytic cardiac arrest secondary to renal tubular acidosis precipitated by severe hyperkalemia. Renal tubular acidosis (RTA) type 4 results from defective distal tubular (DT) response to aldosterone and could lead to hyperkalemia and metabolic acidosis, conditions which in their severe forms, can precipitate cardiac arrest.
Methodology: Here, we present the management of intra-dialysis cardiac arrest precipitated by severe hyperkalemia.
Results: Patient was an 18 year old female, diabetic who had 3 episodes of intra-dialysis cardiac arrest requiring cardiac defibrillation. She was dyspneic, drowsy, pale, had flapping tremor and a tunneled internal jugular catheter insitu. Her pulse was 124/min, blood pressure was 166/98 mmHg and the third heart sounds was heard. Urinalysis showed 3 (+++) of protein. Arterial blood gases (ABGs) revealed hyperkalemia (7.0mmol/l), hypobicarbonatemia (12mmol/l), blood PH (7.2) and blood glucose (249mmol). Serum creatinine was 947umol/l and tall tented T waves were seen on electrocardiogram.
Unique contribution to theory, practice and policy: With a carefully prescribed dialysis, meal and drug regimen, intra-dialysis cardiac arrest can be prevented, and well managed when it occurs.
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References
Kamel KS, Halperin ML. Intrarenal urea recycling leads to a higher rate of renal excretion of potassium: an hypothesis with clinical implications. Curr Opin Nephrol Hypertens 2011; 20:547-54. 10.1097/ MNH.0b013e328349b8f9
Makar MS, Pun PH. Sudden Cardiac Death Among Hemodialysis Patients. Am J Kidney Dis 2017; 69(5): 684-695 10. 1053/j.ajkd.2016.12.006
Bello CHPRT, Duarte JS, Vasconcelos C. Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review. J Bras Nefrol. 2017; 39(4): 481-485 10.5935/0101-2800.2017/0086
Yaxley J, Pirrone C. Review of the Diagnostic Evaluation of Renal Tubular Acidosis. Ochsner J. 2016; 16(4): 525-530.
Ham LL, Nakhoul N, Hering-Smith KS. Acid-Base Homeostasis. Clin J Am Soc Nephrol 2015; 10(12): 2232-2242 10.2215/CJN.0400715
Uduagbamen PK. Acid Base Imbalance in Dialysis: Risk Factors and Impact on Intradialysis Blood Pressure Changes in a Low Income Setting. Findings from a Single Center Prospective Study in Nigeria. Nat J Health Sci 2021; 6(2): 53-60 doi.org/10.21089/njhs.62.0053.
Gumz ML, Lynch IJ, Greenlee MM, Cain BD, Wingo CS. The renal H+K+-ATPases: physiology, regulation, and structure Am J Physiol Renal Physiol 2010; 298(1): F12-F21 10.1152/ajprenal.90723.2008
Berend K. Review of the Diagnostic Evaluation of Normal Anion Gap Metabolic Acidosis. Kidney Dis (Basel). 2017; 3(4):149-159. 10. 1159/000479279
Narcisse D, Agarwal M, Kumar A. A Rare Case of Transient Proximal Renal Tubular Acidosis in Pregnancy. Case Reports Nephrol vol. 2017, Article ID1342135 10.1155/2017/1342135
Dobbin SJH, Petrie JR, Lean MEJ, McKay GA. Fludrocortisone therapy for persistent hyperkalaemia. Diabetic. Med. 2017; 34(7): 1005-1008 10.1111/dme.13359.
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