|Year : 2022 | Volume
| Issue : 3 | Page : 123-126
Sudden cardiac death in a case of Crohn’s disease with COVID-19: A case report
Neeraj Kumar1, Subhajit Ghosh2, Abhyuday Kumar2, Sanjeev Kumar3, Prem Kumar4
1 Department of Trauma & Emergency, All India Institute of Medical Sciences, Patna, India
2 Department of Anaesthesiology, All India Institute of Medical Sciences, Patna, India
3 Department of CTVS, All India Institute of Medical Sciences, Patna, India
4 Department of Radiology, All India Institute of Medical Sciences, Patna, India
|Date of Submission||14-Feb-2021|
|Date of Decision||29-Mar-2021|
|Date of Acceptance||10-Jun-2021|
|Date of Web Publication||27-Jun-2022|
Department of Trauma & Emergency, All India Institute of Medical Sciences, Patna
Source of Support: This study received no extramural founding, Conflict of Interest: None
Rationale: The mechanism of sudden cardiac death in COVID-19 can be multifactorial. Cardiac hypersensitivity to 5-ASA therapy leading to myocarditis has been reported in some cases. Cytokine storm syndrome and idiosyncratic reaction with mesalazine use may lead to sudden cardiac death in COVID-19. Use of immunosuppressants in hospitalized COVID-19 patients should be continued with caution, especially in patients with inflammatory bowel disease.
Patient’s concern: A 75-year-old man who was tested positive for SARS-CoV-2 was admitted with a history of shortness of breath for the last two days. He was a known case of Crohn’s disease treated with mesalazine.
Diagnosis: COVID-19 pneumonia with underlying Crohn’s disease leading to sudden cardiac death.
Intervention: Remdesivir, antibiotics, steroids, low molecular weight heparin, tablet zinc, tab vitamin C, and other supportive treatment were started. Because of increased inflammatory markers, itolizumab was given to the patient on the 2nd day.
Outcome: On the 5th day of the intensive care unit, the patient complained of sudden chest pain with respiratory distress leading to bradycardia and asystole and could not be resuscitated.
Lessons: Causes for sudden cardiac death in COVID-19 pneumonia patients with Crohn’s disease is multifactorial. Although mesalazine may be a safe and effective drug in the management of inflammatory bowel disease, it can induce sytokine strom syndrome and idiosyncratic reactions that could be one of the reasons of sudden cardic death. Therefore, we should be aware of its serious and potentially life-threatening complications, especially in COVID-19 infected patients.
Keywords: COVID-19; Sudden cardiac death; Chron’s disease
|How to cite this article:|
Kumar N, Ghosh S, Kumar A, Kumar S, Kumar P. Sudden cardiac death in a case of Crohn’s disease with COVID-19: A case report. J Acute Dis 2022;11:123-6
|How to cite this URL:|
Kumar N, Ghosh S, Kumar A, Kumar S, Kumar P. Sudden cardiac death in a case of Crohn’s disease with COVID-19: A case report. J Acute Dis [serial online] 2022 [cited 2022 Oct 2];11:123-6. Available from: https://www.jadweb.org/text.asp?2022/11/3/123/347781
| 1. Introduction|| |
Inflammatory bowel diseases (IBD) like Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory diseases of the intestines that may present with many venous vascular comorbidities such as deep venous thrombosis or portal vein thrombosis. These chronic systemic inflammations may lead to endothelial dysfunction and platelet aggregation and serve as a precursor to the development of atherosclerosis and coronary artery disease (CAD). As per the literature, SARS-CoV-2 can lead to unfavorable outcomes in elderly patients with comorbidities, for example, cardiovascular dysfunction. Sudden cardiac death (SCD) has emerged as one of the most challenging concerns amid the COVID-19 pandemic. Although the direct causal association between SCD and COVID-19 remains unproven, but some published data may suggest a plausible association.
| 2. Case report|| |
Departmental Ethics Committee, All India Institute of Medical Sciences Patna, Bihar, India, approved the reporting of this case, and the informed consent was obtained from the patient’s relatives.
A 75-year COVID-19 patient was admitted to our intensive care unit because of the shortness of breath for the last 2 days. He was a known case of Crohn’s disease and hypothyroidism and was on tablet mesalamine 1 g and tablet levothyroxine 25 μg daily. He had stable vitals and maintained saturation on the non-rebreathing mask with a reservoir bag. As per our institutional COVID-19 management protocol, remdesivir, antibiotics, steroids, low molecular weight heparin, tablet zinc, tablet vitamin C, and other supportive treatment were started. Because of increased inflammatory markers, itolizumab was given to the patient on the 2nd day. Artery blood gas was within acceptable limits with a PaO2/FiO2 ratio of 121. The normal arterial blood gases were PH of 7.36, PaO2 of 78 mmHg, PaCO2 of 33 mmHg, HCO3 of 21 mmol/L. The chest X-Ray finding was typically suggestive of COVID-19 with patchy areas of ground-glass opacity in the middle and lower zones in the right and middle zone in the left, with normal costophrenic angle [Figure 1]. On the 3rd day, oxygen requirement was further increased, and oxygen saturation dropped below 90% with a respiratory rate of 38-40 rates per minute. He was put on a high-flow nasal oxygenation machine with a FiO2 of 0.8 and with a flow rate of 5 L/ min. On the 4th day, the patient’s condition was improved, and oxygen saturation was maintained between 95%-97% on transnasal high flow oxygen therapy with FiO2 of 0.6 and at a flow rate of 5 L/min. Routine investigations on days three and four were almost normal except for the inflammatory markers which were raised [Table 1]. A day-by-day clinical progression is shown in [Table 2].
|Figure 1: The chest X-ray (AP-view) of a 75-year-old man with COVID-19. White arrows show extensive opacities in bilateral lungs.|
Click here to view
On the 5th day, the patient complained of sudden chest pain with respiratory distress. A 12-lead electrocardiograph was taken which showed no significant ST-segment change, and trop T was negative. 2-D bedside echocardiography did not show any evidence of pulmonary embolism with normal chamber size and normal left ventricular ejection fraction. But the patient immediately went into bradycardia and followed by asystole. Cardiopulmonary resuscitation was initiated promptly per Advanced Cardiac Life Support protocol; all reversible causes, including tension pneumothorax, cardiac tamponade, and electrolyte/metabolic disturbances were ruled out. However, the patient was not revived and was declared dead.
| 3. Discussion|| |
The mechanism of SCD in COVID-19 can be multifactorial. However, it remains difficult to ascertain the most common mechanism involved due to a lack of data. Both tachyarrhythmia and bradyarrhythmia have been reported in COVID-19. Fatal arrhythmias in COVID-19 may also result from hypoxia, cardiac dysfunction, severe systemic inflammatory state, electrolyte derangements, intravascular volume imbalances, and drug side effects. Guo et al. suggested life-threatening arrhythmias have been variably reported from 10% to 16% of patients hospitalized for severe COVID-19, more commonly in the setting of elevated troponin indicating myocardial injury. Some of the proposed causes of sudden cardiac death in COVID-19 are acute myocarditis (stress-induced cardiomyopathy), acute coronary syndrome, hypoxia, pulmonary thromboembolism, coronary thrombosis, stroke, cardiac tamponade, electrolyte imbalance, underlying channelopathies, and drug-induced arrhythmias. Direct arrhythmogenesis by COVID-19 cytokines has a direct electrophysiological effect on the myocardium, IL-6, tumor necrosis factor-α, and IL-1 can prolong ventricular action potential duration. These cytokines may induce cardiac sympathetic system hyperactivation, which can trigger life-threatening arrhythmic events in patients with long QT. In our case, QT/QTc was 348/452 ms, so the possibility of any QTc prolongation was ruled out. The deep vein thrombosis and pulmonary embolism was also ruled out because of normal echocardiography findings with normal d-dimer and prothrombin time.
Studies have found that IBDs are associated with an increased risk of CAD, cerebrovascular diseases, and peripheral arterial diseases. High levels of circulating cytokines and C-reactive protein are characteristic of IBD, and it is therefore expected to contribute to endothelial dysfunction and atherogenesis. The possible causes of increased cardiovascular events in patients with IBD can be raised inflammatory markers, endothelial dysfunction, hypercoagulability, and release of endotoxins and lipoproteins.
The drug mesalazine (5-ASA) is efficacious in active Crohn’s and ulcerative colitis and are generally regarded as a safe and well-tolerated medication. Cardiac hypersensitivity to 5-ASA therapy leading to myocarditis has been reported in some case studies, and the first reported death from myocarditis associated with mesalazine use was in 1990. In documented literature, hypersensitivity appears to be an idiosyncratic reaction rather than dose-dependent due to its occurrence in patients on very low amounts of mesalazine such as 0.5 g a day.
In our case, sudden cardiac death was possibly due to cardiovascular complications caused by cytokine storm syndrome (raised inflammatory markers) and idiosyncratic reaction with mesalazine use. Our patient had a high-risk factor for cardiovascular complications due to COVID-19, IBD, and mesalazine. Mesalazine is very safe and efficacious in the management of inflammatory bowel disease but we should be aware of its serious and potentially life-threatening complications that may occur especially if it has to be used in COVID-19 infected patients.
To sum up, immunosuppressants in hospitalized COVID-19 patients should be continued with caution. There should be a baseline electrocardiograph to check QTc interval and look for other risk markers of tachy or bradyarrhythmias. Metabolic parameters including electrolytes, fluid volume, and acidosis should be actively sought and treated at the earliest possible, especially in the ICU. Every patient deserves risk stratification based on his/her clinical background with complete available information.
Conflict of interest statement
The authors report no conflict of interest.
This study received no extramural founding.
N.K.: Manuscript writing, proofreading, and final drafting; S.G.: Case management; manuscript writing A.K.: Final drafting; S.K.: Proofreading; P.K.: Proofreading.
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[Table 1], [Table 2]