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 Table of Contents  
Year : 2022  |  Volume : 10  |  Issue : 2  |  Page : 112-119

Recurrent syncope with hyponatremia as presentation of COVID-19 viral pneumonia: Case report

1 Pulmonary Medicine, MIMSR Medical College, India
2 Internal Medicine, MIMSR Medical College, Latur, Maharashtra, India

Date of Submission31-Jan-2022
Date of Decision10-Mar-2022
Date of Acceptance23-Apr-2022
Date of Web Publication19-Dec-2022

Correspondence Address:
Shital Patil
Pulmonary Medicine, MIMSR Medical College,
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jacp.jacp_1_22

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Syncope is the most common neurological presentation in intensive care setting and has diverse etiological factors ranging from ischemic and nonischemic neurovascular, cardiac dysfunction related, infectious, electrolyte imbalance, inflammatory factors to simple viral fever, and other system-related illnesses. Coronavirus disease-19 (COVID-19) is known to cause pulmonary and extrapulmonary complications including effects on cardiovascular, gastrointestinal, renal, and neurovascular systems. In this case report, we have documented a 70-year-old male presented with recurrent syncope with flu-like illness, HRCT thorax suggestive of pneumonia involving bilateral lower lobe, COVID-19 real-time polymerase chain reaction (RT-PCR) positive, with abnormal laboratory parameters such as platelet count, CRP, serum sodium, and vitamin B12 level. Further investigations such as echocardiography, MRI brain and MRI angiography, and carotid Doppler were inconclusive. We have observed excellent clinical and radiological response to steroids, anticoagulants, antiplatelets, and remdesivir with other supportive care in critical care unit.

Keywords: COVID-19 pneumonia, hyponatremia, syncope, viral pneumonia

How to cite this article:
Patil S, Gondhali G. Recurrent syncope with hyponatremia as presentation of COVID-19 viral pneumonia: Case report. J Assoc Chest Physicians 2022;10:112-9

How to cite this URL:
Patil S, Gondhali G. Recurrent syncope with hyponatremia as presentation of COVID-19 viral pneumonia: Case report. J Assoc Chest Physicians [serial online] 2022 [cited 2023 Apr 1];10:112-9. Available from: https://www.jacpjournal.org/text.asp?2022/10/2/112/364436

  Introduction Top

Coronavirus disease-19 (COVID-19) pneumonia is a heterogeneous disease with variable effects on lung parenchyma, airways, and vasculature leading to long-term effects on lung functions. Although lung is the primary target organ involved in COVID-19, many patients have shown pulmonary and extrapulmonary manifestations of various diseases during first and second wave, which occurred as resultant pathophysiological effects of immune activation pathway and direct virus-induced lung damage.[1]

Syncope is a loss of consciousness characterized by a sudden onset, short duration, and spontaneous recovery, which is caused by decreased blood flow in various situations. Syncope can be observed after viral infection, due to prolonged bed rest, lack of sleep, dehydration with high fever, or by direct involvement of cardiac or nervous system. However, the exact mechanism is not clarified.

  Case Summary Top

A 70-year-old male, businessman by occupation, no addiction history, hypertensive, nondiabetic, referred to our center by family physician for recurrent transient loss of consciousness and fever, received symptomatic treatment at peripheral setting.

Further clinical details suggestive of recurrent syncope on three occasions during 5 days, fever which was high grade, intermittent, without chills and rigors, and associated with body ache and headache were seen.

Clinical examination

Heart rate: 100/min; respiratory rate: 26/bpm; blood pressure (BP): 120/70 mm Hg.

oxygen saturation (SpO2): 91% to 94% at room air resting and 89% to 91% at room air on exertion.

Respiratory system examination revealed bilateral breath sounds (normal); basal crepitation’s heard on both lung fields.

Nervous system examination revealed higher functions (normal); no neurological abnormality was observed; cranial nerves were normal; while recent and past memory recall was normal.

Cardiovascular and gastrointestinal systems were normal.

Laboratory examination

Hemoglobin: 10 g%; total white blood cells: 4000/mm3; polymorphs: 65%; platelet count: 132,000/μL.

9C-reactive protein (CRP): 190 mg/L (0–6 mg/L); random blood sugar level: 134 mg%; glycated hemoglobin (HbA1C): 5.60%.

lactate dehydrogenase (LDH): 980 IU/L (70–470 IU/L); uric acid: 3.4 mg (3.5–7.5 mg/dL).

Serum electrolytes – sodium: 129 meq/L (135–145 meq/L); potassium: 3.9 meq/L (3.5–5.5 meq/L); ionic calcium: 1.32 meq/L (1.09–1.36 meq/L).

D-dimer: 193 ng/mL (<500 ng/mL).

Interleukin (IL)-6: 1.75 pg/mL (0.00–7.00 pg/mL).

Thyroid functions: normal.

Vitamin B12 level: 84.2 pg/mL (173–700 pg/mL).

Liver and kidney functions: normal.

Chest X-ray revealed bilateral lower zone infiltrates [Figure 1] and electrocardiogram was suggestive of sinus rhythm [Figure 2].
Figure 1 Chest X-ray Posterio-anterior (PA).

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Figure 2 electrocardiogram (ECG).

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As clinical findings and chest X-ray were suggestive of bilateral lung lower lobe pathology, we recommended for high resolution computerised tomography (HRCT) thorax. HRCT thorax suggestive of compuetrsied tomography (CT) severity 9/25 (0–25) and CORADS-5.

[Figure 3] and [Figure 4] show HRCT thorax suggestive of bilateral basal, peripheral subpleural consolidations, and patchy confluent multifocal ground glass opacifications (GGOs).
Figure 3 HRCT thorax showing right lower lobe consolidation.

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Figure 4 HRCT thorax showing right lower lobe ground glass opacities and consolidation.

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[Figure 5] and [Figure 6] show HRCT thorax suggestive of bilateral basal, peripheral subpleural consolidations [Figure 5] and patchy confluent multifocal GGOs predominant on right side [Figure 6], respectively.
Figure 5 HRCT thorax showing bilateral multifocal, peripheral, subpleural lower lobe ground glass opacities and consolidation.

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Figure 6 HRCT thorax showing right middle lobe multifocal consolidations.

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[Figure 7],[Figure 8],[Figure 9],[Figure 10] show HRCT thorax suggestive of bilateral basal, peripheral subpleural consolidations, and patchy confluent GGOs predominant on lower lobes.
Figure 7 HRCT thorax showing bilateral multifocal lower lobe ground glass opacities and consolidation.

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Figure 8 HRCT thorax showing right lower lobe peripheral, subpleural, ground glass opacities and consolidation.

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Figure 9 HRCT thorax showing right lower lobe peripheral, subpleural, ground glass opacities.

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Figure 10 HRCT thorax showing right lower lobe peripheral, subpleural, linear and ground glass opacities.

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As patient was referred by general physician for fever and syncope, we have taken teleconsultation of a neurologist. After complete neurological examination history, the neurophysician advised for magnetic resoanance imaging (MRI) brain, MRI brain angiography, carotid artery Doppler bilateral neck, and 2D echocardiography.

MR angiography documented normal cerebral and vertebral circulation. Also, stenosis or luminal abnormality were not documented [Figure 11],
Figure 12 MRI angiography showing normal perfusion in cerebral vessels and circle of willis.

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,[Figure 13].
Figure 11 MRI angiography showing normal perfusion in cerebral vessels.

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{Figure 12}
Figure 13 MRI angiography vertebral and circle of Willis vessels.

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MRI brain suggestive of mild chronic ischemic changes was seen in bilateral frontoparietal subcortical and periventricular white matter [Figure 14],
Figure 15 MRI brain suggestive of mild chronic ischemic changes in bilateral frontoparietal subcortical and periventricular white matter No acute infarct seen.

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Figure 16 MRI brain showing diffuse hyperintensity in bilateral frontoparietal subcortical and periventricular white matter indicates deep small vessel ischemia.

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Figure 14 MRI brain shwoing normal third and fourth ventricles, prominent cortical sulci and cisternal spaces.

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{Figure 15}{Figure 16}

Carotid Doppler suggestive of bilateral common carotid artery, internal carotid artery, external carotid artery with mild calcified atherosclerotic stenosis was observed. Origins of both carotid artery were normal.

2D echocardiography: normal chamber size, good left ventricular functions, no regional wall motion abnormality (i . e., no type I diastolic dysfunction). Normal valves, no MR or pulmonary arterial hypertension (PAH).

As HRCT thorax suggestive of CT severity 9/25 (0–25) and CORADS-5, bilateral basal, peripheral subpleural consolidations and patchy confluent multifocal GGOs, we have sent COVID-19 workup.

COVID-19 RT PCR (Real-Time Reverse Transcription ? Polymerase Chain) test and results documented positive for severe acute respiratory syndrome-corona virus (SARS-CoV-2).

We have documented hyponatremia, decreased vitamin B12 level, COVID-19 pneumonia and viremia or increased inflammatory markers as reasons for syncope.

We have started anticoagulation with low-molecular-weight heparin (LMWH injection 60 units BID, injection methylprednisolone 40 mg IV TDS, injection remdesivir, oral formulations of aspirin 75 mg OD, and oxygen supplementation with target SpO2 >95% and other supportive care in indoor unit. Clinical response documented after 48 hours of treatment, with near-complete symptomatic recovery and respiratory, neurological, and cardiovascular parameters were normalized and hematological parameters such as thrombocytopenia and leukopenia were improved after 72 hours of treatment. Dyselectrolytemia (hyponatremia) recovered after 72 hours and sodium level were 138 meq/L (135–145 meq/L) without normal saline use, maybe it has responded to methylprednisolone and we have avoided fluid therapy for COVID patients in our unit unless patient is in hypotension. Inflammatory markers like CRP took 5 days for decrease in titer form 190 mg/L to 12 mg/L. We have discharged patient after neurological recovery and 6 minutes’ walk parameters are acceptable and having saturation more than 96% at room air.

  Discussion Top

Syncope may be a very common chief complaint of patients presenting to the emergency department (ED), with a broad differential diagnosis. Patients with syncope, especially when deemed vasovagal or orthostatic, are usually dismissed from the ED after a thorough clinical history evaluation.[2]

The mechanism behind the occurrence of syncope in COVID-19 has not been described. Syncope due to structural cardiac disease or pulmonary embolism has been ruled out as well. The proposed pathophysiological explanation might be a neurally mediated/reflex mechanism in its nonclassical form (absence of certain trigger) or an autonomic dysfunction, either primary or secondary. There are two main pathophysiological mechanisms in reflex syncope, both of them depending on an imbalance between sympathetic and parasympathetic activity: vasodepression, caused by insufficient sympathetic vasoconstriction; and cardioinhibition, caused by parasympathetic predominance. This type of imbalance might find another confirming factor in the association between COVID-19 infection and “inappropriate” sinus tachycardia, which often characterizes patients with novel coronavirus infection even in the absence of respiratory failure.[3]

The autonomic failure hypothesis, on the other hand, might involve a primary failure caused by the virus itself or a secondary failure due to autoimmune autonomic neuropathy. The occurrence of neurologic features in COVID-19 infection has been recently documented, in terms of encephalopathy and corticospinal tract involvement.[4],[5] However, determining if this is a direct effect of the virus or if it is due to a critical autoimmune reaction or inflammation caused by cytokines is still a matter of debate. Cytokine storm with subsequent hyperinflammation is one of the proposed mechanisms of COVID-19 serious illness.[6] Vascular injury caused by IL-1 and IL-6 and decreased systemic vascular resistance resulting in vasodilation could be one of the possible explanations of syncope as the resulting symptom.[5],[6]

The hyponatremia (as defined as plasma sodium <135 mmol/L) is the most common electrolyte disorder with a prevalence as high as 30% in inpatient settings.[7] In COVID-19, hyponatremia is common and its etiology is not clear, probably is multifactorial not only be associated with pneumonia but also with the gastrointestinal symptoms of this infection and could appears to be outside the kidneys, as it happens in syndrome of inappropriate secretion of antidiuretic hormone (SIADH).[7] The most common cause of hyponatremia is the SIADH, which accounts for up to 40% to 50% of cases, but the prevalence may be higher in some pathological conditions, such as subarachnoid hemorrhage, traumatic brain injury, and pneumonia. However, it can be assumed that data from other collectives with community-acquired pneumonia or from critically ill patients can be extrapolated.[7]

It is unclear whether hyponatremia due to SIADH is common in this population. Probably, hyponatremia is a direct consequence of glucocorticoid deficiency caused by insufficient hypothalamic–pituitary stimulation. Furthermore, it may be related to an inappropriate antidiuresis resulting from nonsuppressible arginine vasopressin release (despite hypoosmolality) and, probably, to a direct renal water excretion defect, both being consequences of cortisol deficiency, but with an intact renin–angiotensin–aldosterone system.[8] In the vast majority of reported cases, the hyponatremia appeared after a digestive episode and respiratory infection. The association of hyponatremia and COVID-19 infection with endocrine disorders has been described in recent studies, although the possible underlying pathophysiological mechanisms are not known currently, we do not have any such data on cortisol dynamics in patients with COVID-19.[8] Sixty-one survivors of SARS were evaluated at 3 months postrecovery and thereafter periodically. Forty percent of patients had evidence of central hypocortisolism, most of them (62.5%) were resolved within a year. The authors had proposed the possibility of a reversible hypophysitis or a direct hypothalamic damage that could have led to a state of hypothalamic-pituitary dysfunction.[9],[10]

In our case, we have documented hyponatremia as probable cause for recurrent syncope and responded very excellently to steroids; other plausible mechanism were: decreased B12 level, gastrointestinal symptoms secondary to COVID-19, inflammatory surge leading to SIADH-like pathophysiology.

Key learning points from this case report

  1. COVID 19 disease is known to cause pulmonary and extrapulmonary complications including effects on cardiovascular, gastrointestinal, renal, and neurovascular systems.
  2. Although syncope is a vague neurological manifestation of many neurological and non-neurological illnesses, it is well documented in viral illnesses such as flu and COVID; recurrent syncopal episodes need further workup.
  3. Neurovascular complications such as stroke, venous thrombosis, encephalopathy, and vasculitis are documented in various studies.
  4. We have documented, dyselectrolytemia as result of pulmonary involvement in COVID-19 disease is reason for recurrent syncope. We have also documented decreased B12 level as other nutritional factor which has exacerbated recurrent syncope.
  5. Early interventions such as, timely steroid use has positive impact on both COVID pneumonia and neurological outcome and anticoagulation with antiplatelets have a crucial role in early clinical recovery.
  6. Steroids are cornerstone of treatment of recurrent syncope due to hyponatremia secondary to probable SIADH-like pathology due to viral lung pneumonia process; and have shown excellent response in the form of sodium recovery irrespective of external salt correction; and also shown lung pathology improvement after steroid use.
  7. We recommend, all cases with recurrent syncope should undergo HRCT thorax in current scenario of COVID-19 pandemic as many of these cases may have less respiratory symptoms as compared to extrapulmonary symptoms, and in these cases with SpO2 <93% warrants lung pathology to be ruled out to have satisfactory treatment outcome.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Shital P, Gondhali G. Does genetic makeup of corona virus in COVID-19 disease is as predicted or is similar to other respiratory viruses like influenza? Still, we believe in covid appropriate behavior in spite of vaccination……Show must go on! Saudi J Med 2022;7:1–3.  Back to cited text no. 1
Brignole M, Moya A, de Lange FJ, Deharo JC, Elliott PM, Fanciulli A et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J 2018;39:1883–1948.  Back to cited text no. 2
Ebrille E, Lucciola MT, Amellone C, Ballocca F, Orlando F, Giammaria M. Syncope as the presenting symptom of COVID-19 infection. HeartRhythm Case Rep 2020;6:363–6. doi:https://doi.org/10.1016/j.hrcr.2020.04.015  Back to cited text no. 3
Asadi-Pooya AA, Simani L. Central nervous system manifestations of COVID-19: A systematic review. J Neurol Sci 2020;413:116832.  Back to cited text no. 4
Helms J Kremer S, Merdji H, Clere-Jehl R, Schenck M, Kummerlen C et al. Neurologic features in severe SARS-CoV-2 infection. N Engl J Med 2020;382:2268–70. doi: https://doi.org/10.1056/NEJMc2008597  Back to cited text no. 5
McGonagle D, Sharif K, O’Regan A, Bridgewood C. The role of cytokines including interleukin-6 in COVID-19 induced pneumonia and macrophage activation syndrome-like disease. Autoimmun Rev 2020;19:102637.  Back to cited text no. 6
De La FLor JC, Marschall A, Biscotti B, Rodeles del Pozo M. Hyponatremia in COVID-19 infection: Should only think about SIADH. J Clin Nephrol Ren Care 2020;6:57. doi.https://doi.org/org/10.23937/2572-3286.1510057  Back to cited text no. 7
Reynolds RM, Seckl JR. Hyponatraemia for the clinical endocrinologist. Clin Endocrinol (Oxf) 2005;63:366–74.  Back to cited text no. 8
Leow MK, Kwek DS, Ng AW, Ong KC, Kaw GJ, Lee LS. Hypocortisolism in survivors of severe acute respiratory syndrome (SARS). Clin Endocrinol (Oxf) 2005;63:197–202.  Back to cited text no. 9
Gu J, Gong E, Zhang B, Zheng J, Gao Z, Zhong Y et al. Multiple organ infection and the pathogenesis of SARS. J Exp Med 2005;202:415–24.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16]


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