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Brugada Pattern in Diabetic Ketoacidosis: A Case Report and Scoping Study

Syed Haseeb, Pramod Theetha Kariyanna, Apoorva Jayarangaiah, Ganesh Thirunavukkarasu, Sudhanva Hegde, Jonathan D. Marmur, Sneha Neurgaonkar, Samy I. McFarlane
American Journal of Medical Case Reports. 2018, 6(9), 173-179. DOI: 10.12691/ajmcr-6-9-2
Received August 05, 2018; Revised September 10, 2018; Accepted October 07, 2018

Abstract

Brugada syndrome is a rare cardiac arrhythmia which is associated with right bundle branch block pattern (RBBB) and ST-segment elevation in right precordial leads. SCNA5 mutation is the most common genetic abnormality associated with Brugada syndrome. Brugada pattern not related to genetic mutations has been previously reported in the setting of fever, metabolic conditions, lithium use, marijuana and cocaine abuse, ischemia and pulmonary embolism, myocardial and pericardial diseases. Multiple isolated cases of Brugada pattern associated with diabetic ketoacidosis (DKA) have been previously reported. We here present a case of type 1 Brugada pattern in a 23 year-old-male who presented with DKA. Brugada pattern in DKA is attributed to acidosis and multiple electrolyte abnormalities including hyperkalemia which alter ion channel expression in the heart thus leading to Brugada pattern which subsequently resolved with treatment of DKA. In such patients, Brugada pattern is not reproducible on procainamide induction cardiac electrophysiology study (EPS). Our scoping study demonstrates male predominance 20/22 cases of (DELETE this highlighted area) Brugada pattern in DKA, a finding that is consistent with prevalence of this disease among males.

1. Introduction

Brugada syndrome is a rare cardiac arrhythmia which is associated with right bundle branch block pattern (RBBB) and ST-segment elevation in right precordial leads 1. Brugada Syndrome is associated with life-threatening arrhythmias and/or sudden cardiac death in the absence of underlying structural heart disease 1. The overall prevalence of a Brugada type electrocardiogram in the United States is approximately 0.43%. It is a familial syndrome that is more likely to present in males. Interestingly male to female disease presentation was noted to be higher in Japan compared to the United States at 9: 1 and 2: 1 ratios respectively 2, 3, 6. Multiple genetic mutations have been isolated in cardiac sodium, potassium, calcium, and protein regulatory channels; it is most commonly attributed to one gene: SCN5A, which encodes an α-subunit of a sodium channel, in an autosomal dominant pattern of inheritance 4, 5.

Brugada pattern can be “induced” by administration of sodium channel blockers such as flecainide, procainamide, and ajmaline 6. One international registry lists Brugada pattern in patients with metabolic conditions, mechanical compression, ischemia and pulmonary embolism, myocardial and pericardial disease, and ECG modulation 7. Furthermore, Brugada pattern has been noted in patients in Diabetes Ketoacidosis (DKA) in the setting of extreme electrolyte disturbances including hyperkalemia, hyponatremia, hyperglycemia, and acidosis; it resolves with the appropriate and timely management of the DKA 8. Flecainide, a potent class IC antiarrhythmic, failed to successfully “induce” Brugada in a case which initially presented with this pattern in the setting of DKA 8. We here present a case of DKA with a Brugada pattern on initial ECG which resolved with treatment of DKA and underlying electrolyte disturbances, serial ECGs performed showed a rapid resolution of this pattern.

2. Case Report

A 23-year-old Afro-Caribbean male with a past medical history of tobacco use and type 1 Diabetes Mellitus since nine years of age presented with DKA. Patient’s diabetes was managed by continuous insulin infusion for nine years however he reported non-adherence due to insulin pump malfunction over the past week. He reported nausea, several episodes of vomiting, fatigue, polydipsia, and a non-productive cough at home without any polyuria or dysuria at the time of presentation.

On arrival patient’s vitals presented as blood pressure of 103/52 mm Hg, heart rate of 110 beats per min, afebrile, respiring at 30 breaths per minute saturating 92%. On physical exam, the patient appeared lethargic with labored breathing. The laboratory findings on the day of admission are summarized in Table 1.

Admission electrocardiogram revealed atrial fibrillation, right bundle branch block (RBBB), and coved ST-segment elevations in leads V1-V3 consistent with a Brugada pattern (image 1). A bedside echocardiogram showed no wall motion or valvular abnormalities, no pericardial effusion, and the ejection fraction was estimated to be 60%.

The patient was treated for DKA with subsequent resolution of hyperkalemia, hyponatremia, hyperglycemia, and metabolic acidosis. Initial labs revealed sodium 103 mmol/L, potassium 8.6 mmol/L, random blood sugar 1313 mg/dl, bicarbonate 5.5 mmol/L, blood urea nitrogen 62 mg/dl, and serum creatinine as 2.69 mg/dl. Repeat labs within 6-9 hours of admission showed significant improvement as shown in Table 1. ECG performed within two hours demonstrated complete resolution of atrial fibrillation and the Brugada pattern. The day after presentation the patient’s ECG has returned completely to baseline with complete resolution of all changes and his labs improved further to Na 134 mmol/l, K 4.1 mmol/l, random blood sugar 259 mg/dl, bicarbonate 11 mmol/l, blood urea nitrogen 48 mg/dl, creatinine 1.78 mg/dl. He did not have any life-threatening arrhythmias on telemetry monitoring and subsequent imaging with a transthoracic echocardiogram showed no structural changes. CHA2DS2-VASc Score for atrial fibrillation stroke risk was calculated as one and therefore anticoagulation was not initiated after discussing risks and benefits with the patient.

3. Discussion

Brugada pattern is a unique entity, unlike Brugada syndrome, where certain physiologic changes can predispose to life-threatening arrhythmias and sudden cardiac death in the absence of known underlying genetic mutations and/or structural heart disease. Though it is not clear why patients in DKA develop a Brugada pattern, the proposed mechanism revolves around inactivation of the cardiac sodium channels secondary to hyperkalemia and acidosis 9. Male predominance can be attributed to a more prominent outward current-mediated action potential found in the right ventricular epicardium of males 9. The pattern resolves immediately with the treatment of the underlying disturbance associated with DKA and was seen within two hours of treatment in our case. Table 3 lists a number of similar cases where Brugada pattern presented after an initial presentation of DKA.

Other potential triggers of Brugada pattern are summarized by cases in Table 2. There has been a high prevalence in a patient diagnosed with schizophrenia, however, the association was not found to have a correlation with sodium channel blocking medications often prescribed in schizophrenia 10. Febrile states have been theorized to modulate sodium channels and provoke Brugada syndrome perhaps through missense mutations of T1620M 11 and several cases have been reported to date 12, 13, 14, 15, 16. Illicit drugs such as cocaine and marijuana have been listed as triggers. Cocaine a potent sympathomimetic was isolated as a trigger in two case reports with one case repeatedly presenting with Brugada pattern within 2-5 days of cocaine use. Mechanisms have been proposed to involve both increases in overall norepinephrine and sodium blocking properties predisposing to arrhythmias 17, 18. Marijuana’s proposed mechanism is due to vagal stimulation by cannabis which has previously seen to trigger Brugada Syndrome 19, 20, 21, 22. Medication use with SSRI and Lithium as triggers have been reported as well. Both medications are potent blockers of cardiac sodium channels and can provoke Brugada syndrome in patients 23, 24, 25, 26, 27. Medication overdose including diphenhydramine and tricyclic antidepressant has been isolated as triggers of arrhythmias and proposed mechanism is attributed anticholinergic overactivity 28, 29. One reported case has found a rare complication of hemopericardium and tumor formation from underlying rheumatoid arthritis which compressed the ventricle and unmasked a Brugada pattern 30. Adrenocortical insufficiency which is commonly associated with hyperkalemia can decrease resting membrane potential inactivating cardiac sodium channels and produce similar findings 31.

In our case, the Brugada pattern was elucidated in diabetic ketoacidosis with hyperkalemia and acidosis. In Table 3, we have reviewed 22 case reports that presented with a Brugada pattern in DKA initially concerning for a myocardial infarction. Similar to our case, the pattern resolved with the timely management of the underlying electrolyte disturbances. Furthermore, our review re-demonstrated a male predominance at a ~7.33: 1 male-female ratio with ages ranging from 7 to 72. Mean and median values were calculated for age, pH, glucose, sodium, potassium, and bicarbonate levels. The average age was found to be ~45.9 years, average pH on admission at 7.054, average glucose 958.7 mg/dl, average potassium for 7.424 mmol/L, average sodium 123.6 mmol/L, and average bicarbonate to be 7.7 mmol/L. Our case showed that our patient was lower than average in age, pH, and bicarbonate levels and greater than average in potassium and glucose levels. Some of the cases evaluated the cardiac function with transthoracic echocardiograms and they demonstrated no structural or valvular abnormalities which were consistent with our own echocardiogram findings. Others performed cardiac catheterization with normal coronaries. All cases had complete recovery once the DKA was treated and they bring to attention great importance in the close outpatient follow-up of diabetic management.

4. Conclusion

DKA may precipitate Brugada pattern in middle-aged men with no genetic predisposition. Brugada pattern will completely resolve on appropriate management of DKA. Acidosis and hyperkalemia in DKA promote electrophysiologic changes in the cardiac sodium channels producing a Brugada pattern/ coved ST-elevation mimicking acute myocardial infarction on an ECG. Brugada induction in electrophysiology laboratory often fails to induce Brugada pattern in such patients suggesting the Brugada pattern in these patients is due to DKA.

Acknowledgements

This work is sponsored in part by the Brooklyn Health Disparities Center NIH grant #P20 MD006875.

References

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In article      
 
[2]  Monroe MH, Littmann L. Two-year case collection of the Brugada syndrome electrocardiogram pattern at a large teaching hospital. Clinical cardiology. 2000 Nov; 23(11): 849-51.
In article      View Article  PubMed
 
[3]  Bezzina CR, Rook MB, Wilde AA. Cardiac sodium channel and inherited arrhythmia syndromes. Cardiovascular research. 2001 Feb 1; 49(2): 257-71.
In article      View Article
 
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In article      View Article  PubMed
 
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In article      View Article  PubMed
 
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In article      View Article
 
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In article      View Article  PubMed
 
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In article      View Article  PubMed
 
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In article      View Article  PubMed
 
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In article      
 
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In article      View Article  PubMed
 
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In article      
 
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Published with license by Science and Education Publishing, Copyright © 2018 Syed Haseeb, Pramod Theetha Kariyanna, Apoorva Jayarangaiah, Ganesh Thirunavukkarasu, Sudhanva Hegde, Jonathan D. Marmur, Sneha Neurgaonkar and Samy I. McFarlane

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Cite this article:

Normal Style
Syed Haseeb, Pramod Theetha Kariyanna, Apoorva Jayarangaiah, Ganesh Thirunavukkarasu, Sudhanva Hegde, Jonathan D. Marmur, Sneha Neurgaonkar, Samy I. McFarlane. Brugada Pattern in Diabetic Ketoacidosis: A Case Report and Scoping Study. American Journal of Medical Case Reports. Vol. 6, No. 9, 2018, pp 173-179. http://pubs.sciepub.com/ajmcr/6/9/2
MLA Style
Haseeb, Syed, et al. "Brugada Pattern in Diabetic Ketoacidosis: A Case Report and Scoping Study." American Journal of Medical Case Reports 6.9 (2018): 173-179.
APA Style
Haseeb, S. , Kariyanna, P. T. , Jayarangaiah, A. , Thirunavukkarasu, G. , Hegde, S. , Marmur, J. D. , Neurgaonkar, S. , & McFarlane, S. I. (2018). Brugada Pattern in Diabetic Ketoacidosis: A Case Report and Scoping Study. American Journal of Medical Case Reports, 6(9), 173-179.
Chicago Style
Haseeb, Syed, Pramod Theetha Kariyanna, Apoorva Jayarangaiah, Ganesh Thirunavukkarasu, Sudhanva Hegde, Jonathan D. Marmur, Sneha Neurgaonkar, and Samy I. McFarlane. "Brugada Pattern in Diabetic Ketoacidosis: A Case Report and Scoping Study." American Journal of Medical Case Reports 6, no. 9 (2018): 173-179.
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  • Image 1. Patient’s initial ECG: Atrial fibrillation and coved ST-segment elevations with RBBB consistent with a Type 1 Brugada pattern
  • Image 2. ECG obtained two hours after initiation of DKA management showing conversion into normal sinus rhythm and resolution of Brugada pattern
  • Figure 1. Trends of sodium, potassium, glucose, and bicarbonate levels (white arrow indicating time line at which Brugada pattern resolved)
[1]  Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, Corrado D, Hauer RN, Kass RS, Nademanee K, Priori SG. Proposed diagnostic criteria for the Brugada syndrome. European Heart Journal. 2002 Nov; 23(21): 1648.Patel SS, Anees SS, Ferrick KJ. Prevalence of a Brugada pattern electrocardiogram in an urban population in the United States. Pacing and Clinical Electrophysiology. 2009 Jun; 32(6): 704-8.
In article      
 
[2]  Monroe MH, Littmann L. Two-year case collection of the Brugada syndrome electrocardiogram pattern at a large teaching hospital. Clinical cardiology. 2000 Nov; 23(11): 849-51.
In article      View Article  PubMed
 
[3]  Bezzina CR, Rook MB, Wilde AA. Cardiac sodium channel and inherited arrhythmia syndromes. Cardiovascular research. 2001 Feb 1; 49(2): 257-71.
In article      View Article
 
[4]  Brugada R, Brugada J, Antzelevitch C, Kirsch GE, Potenza D, Towbin JA, Brugada P. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation. 2000 Feb 8; 101(5): 510-5.
In article      View Article  PubMed
 
[5]  Brugada R, Campuzano O, Sarquella-Brugada G, Brugada J, Brugada P. Brugada syndrome. Methodist DeBakey cardiovascular journal. 2014 Jan; 10(1): 25.
In article      View Article  PubMed
 
[6]  Matsuo K, Akahoshi M, Nakashima E, Suyama A, Seto S, Hayano M, Yano K. The prevalence, incidence and prognostic value of the Brugada-type electrocardiogram: a population-based study of four decades. Journal of the American College of Cardiology. 2001 Sep 1; 38(3): 765-70.
In article      View Article
 
[7]  Anselm DD, Gottschalk BH, Baranchuk A. Brugada phenocopies: consideration of morphologic criteria and early findings from an international registry. Canadian Journal of Cardiology. 2014 Dec 1; 30(12): 1511-5.
In article      View Article  PubMed
 
[8]  Kovacic JC, Kuchar DL. Brugada pattern electrocardiographic changes associated with profound electrolyte disturbance. Pacing and clinical electrophysiology. 2004 Jul; 27(7): 1020-3.
In article      View Article  PubMed
 
[9]  Littmann L, Monroe MH, Taylor III L, Brearley Jr WD. The hyperkalemic Brugada sign. Journal of electrocardiology. 2007 Jan 1; 40(1): 53-9.
In article      View Article  PubMed
 
[10]  Blom MT, Cohen D, Seldenrijk A, Penninx BW, Nijpels G, Stehouwer CD, Dekker JM, Tan HL. Brugada syndrome ECG is highly prevalent in schizophrenia. Circ Arrhythm Electrophysiol. 2014 Jun 1; 7(3): 384-91.
In article      View Article  PubMed
 
[11]  Antzelevitch C, Brugada R. Fever and Brugada syndrome. Pacing and Clinical Electrophysiology. 2002 Nov; 25(11): 1537-9.
In article      View Article  PubMed
 
[12]  González JR, Hernández AM, Garcia A, de Castro García A, Mejias A, Moro C. Recurrent ventricular fibrillation during a febrile illness in a patient with the Brugada syndrome. Revista espanola de cardiologia. 2000 May; 53(5): 755-7.
In article      
 
[13]  Madle A, Kratochvil Z, Polivkova A. The Brugada syndrome. Vnitrni lekarstvi. 2002 Mar; 48(3): 255-8.
In article      PubMed
 
[14]  Saura D, GARCÍA‐ALBEROLA AR, Carrillo P, Pascual D, MARTÍNEZ‐SÁNCHEZ JU, Valdes M. Brugada‐like electrocardiographic pattern induced by fever. Pacing and Clinical Electrophysiology. 2002 May; 25(5): 856-9.
In article      View Article  PubMed
 
[15]  PORRES JM, Brugada J, Urbistondo V, Garcia F, Reviejo K, Marco P. Fever unmasking the Brugada syndrome. Pacing and clinical electrophysiology. 2002 Nov; 25(11): 1646-8.
In article      PubMed
 
[16]  Kum LC, Fung JW, Sanderson JE. Brugada syndrome unmasked by febrile illness. Pacing and clinical electrophysiology. 2002 Nov; 25(11): 1660-1.
In article      View Article  PubMed
 
[17]  Ortega-carnicer J, Bertos-polo J, Gutiérrez-tirado C. Aborted sudden death, transient Brugada pattern, and wide Qrs dysrhythmias after massive Cocaine ingestion. Annals of Emergency Medicine. 2003 Mar 1; 41(3): 434-5.
In article      
 
[18]  Littmann L, Monroe MH, Svenson RH. Brugada-type electrocardiographic pattern induced by cocaine. In Mayo Clinic Proceedings 2000 Aug 1 (Vol. 75, No. 8, pp. 845-849). Elsevier
In article      
 
[19]  Doctorian T, Chou E. Cannabis-Induced Brugada Syndrome Presenting as Cardiac Arrest.
In article      
 
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