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MBBS, MD (Pathology),
Sanjay Gandhi institute of trauma and orthopedics,
Bengaluru.
On Aug 2018




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Aug 2018




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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011




Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
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Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011
Anuradha

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.


Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020

Important Notice

Case report
Year : 2022 | Month : June | Volume : 16 | Issue : 6 | Page : OD17 - OD19 Full Version

Hypertension Secondary to COVID-19 Leading to Posterior Reversible Encephalopathy Syndrome in a 13-year-old Male


Published: June 1, 2022 | DOI: https://doi.org/10.7860/JCDR/2022/56337.16512
Saranya Sai Satya Nelabhotla, Pradnya Diggikar, Prashant Gopal

1. Resident, Department of General Medicine, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, Maharashtra, India. 2. Professor, Department of General Medicine, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, Maharashtra, India. 3. Resident, Department of General Medicine, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, Maharashtra, India.

Correspondence Address :
Dr. Prashant Gopal,
Resident, Department of General Medicine, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, Maharashtra, India.
E-mail: drprashantgopal@gmail.com

Abstract

Posterior Reversible Encephalopathy Syndrome (PRES) is a clinico-radiological condition defined by white matter vasogenic oedema predominantly affecting the posterior occipital and parietal lobes. A 13-year-old male presented with complaints of fever for 4 days.Upon evaluation, he turned out positive for COVID-19 with a Computed Tomography (CT) severity score of 5/25. Three days post admission (day 7 of illness), patient developed sudden onset of painless, diminution of vision in both eyes followed by two episodes of generalised tonic clonic seizures. Examination revealed a blood pressure of 180/110 mmHg. Characteristic Magnetic Resonance Imaging (MRI) findings led to a diagnosis of PRES. Patient was treated with antiepileptics, antihypertensives and intravenous mannitol and made a complete recovery. Early identification, treatment of symptomatology and correction of the underlying cause are all key aspects of management.

Keywords

Anticonvulsive agents, Convulsive generalised seizure disorder, High blood pressure, Reversible cortical blindness, Vasogenic cerebral oedema

Case Report

A13-year-old male with no significant medical history presented with complaints of fever for four days. Fever was continuous, high grade and relieved on taking over the counter medications. There was no history of cold, cough, breathlessness, palpitations, chest pain, pain in abdomen, headache or burning micturition. Patient was not vaccinated against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). His father and maternal uncle were both diagnosed with COVID-19 infection seven days earlier.

General examination revealed a Blood Pressure (BP) of 130/80 mmHg, Heart Rate of 96 beats per minute (bpm), respiratory rate of 16 cycles/minute, oxygen saturation of 97% at room air. All peripheral pulses were normal. Systemic examination revealed no abnormalities. Laboratory investigations revealed raised inflammatory markers and negative fever profile (Table/Fig 1).

Test for COVID-19 Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was positive. Patient was started on tab. paracetamol 500 mg and intravenous fluids. Steroids and antivirals were not started due to the mild nature of the disease. High-Resolution Computed Tomography (HRCT) thorax revealed bilateral peripheral basal consolidations with a Computed Tomography (CT) severity score of 5/25.

Patient was continued on symptomatic treatment and three days post admission, patient complained of painless sudden onset diminution of vision in both eyes associated with headache which was occipital and throbbing in nature. Patient was conscious, oriented and obeying commands. There was complete loss of vision in both eyes with no perception of light and projection of rays bilaterally. Ocular and fundus examination was normal. Pupil examination revealed normal accommodation and light reflexes. Intraocular pressure was normal. Examination revealed a BP reading of 180/110 mmHg. Two hours later, patient developed two episodes of generalised tonic clonic seizures.Patient was unaware of these episodes and postictal confusion lasted for a few minutes with no bowel or bladder involvement. Kernig’s and Brudzinski’s were negative. Neurological examination revealed bilateral extensor plantar response. Cranial nerves, motor, sensory and deep tendon reflexes examination were normal.

An initial differential diagnosis of ischemic stroke, cerebral haemorrhage, Cerebral Venous Sinus Thrombosis (CVST) and Posterior Reversible Encephalopathy Syndrome (PRES) was considered due to the abrupt onset of headache and bilateral vision loss with elevated blood pressure.

Cerebrospinal fluid analysis was normal. Neuroimaging {Magnetic Resonance Imaging (MRI) of brain with angiography and venography-plain and contrast} revealed T2-weighted Fluid Attenuated Inversion Recovery (T2/FLAIR) hyperintensities and corresponding T1WI hypointensities involving the cortical and subcortical white matter of bilateral parietal, occipital lobes and bilateral cerebellar hemispheres indicating vasogenic oedema suggestive of PRES (Table/Fig 2).

Creatine kinase-MB (CK-MB) (112 IU/L) and cardiac Troponin-I (44 IU/L) were elevated. Electrocardiography (ECG) and 2D-echocardiography were normal. Plasma renin activity, aldosterone levels and plasma free nor metanephrine levels were normal. Renal artery doppler showed no abnormalities.

Based on the above findings, a diagnosis of PRES was made. A normal Cerebrospinal Fluid (CSF) picture and lack of an identifiable cause of hypertension led us to conclude that PRES was secondary to hypertension associated with COVID-19. Patient was started on injection mannitol, antiepileptics (inj levetiracetam 1 gm i.v. stat followed by 500 mg i.v. q12hr) and antihypertensives (tab. amlodipine 5 mg PO q12hr, tab. telmisartan 40mg PO q24hr) anda target blood pressure of 130/80 mmHg was maintained. His vision started to improve on day 4 of admission and completely recovered by day five post admission. A contrast enhanced F-18 Fluorodeoxyglucose (FDG)-Positron Emission Tomography (PET) scan was done which showed mild to moderate hypometabolism in the region of the left sensorimotor cortex and mild hypometabolism in the left precuneus. Rest of the scan was normal.

Inj. mannitol (100 mL i.v. q8hr for 3 days followed by 100 mL i.v. q12hr for 1 day followed by 100 mL IV q24hr for 1 day) and antihypertensives (tab. telmisartan 40 mg q24hr for 5 days, tab. amlodipine 5 mg q12hr for 4 days followed by tab. amlodipine 5 mg q24hr for 5 days) were tapered and stopped by day 11 of admission. Patient was kept under observation for a total of 14 days at the end of which his BP was 130/80 mmHg. Visual acuity was 6/6 at the time of discharge. Patient is asymptomatic on follow-up three months postdischarge.

Discussion

Posterior reversible encephalopathy syndrome is a clinico-radiological condition defined by white matter vasogenic oedema predominantly affecting the posterior occipital and parietal lobes. Hinchey J et al., originally described PRES in 1996 (1). Seizures, loss of consciousness, headaches, visual problems, nausea/vomiting and focal neurological abnormalities are characteristics of this condition (2). It has been reported in individuals ranging from 4 to 90 years, with the majority of cases affecting young to middle-aged adults (3).

Hypertension, pre eclampsia/eclampsia, infections, renal dysfunction, autoimmune diseases such as systemic lupus erythematosus, systemic sclerosis, tumour lysis syndrome, Guillain-Barr syndrome, Acquired Immunodeficiency Syndrome (AIDS), thrombotic thrombocytopenic purpura, and immunosuppressive agents are among the most common causes of PRES, all of which cause cerebral vasogenic oedema, which appears to be the key pathogenic mechanism (4). Stroke, meningoencephalitis, demyelinating diseases of the brain, and cerebral venous sinus thrombosis are all possible differential diagnoses (5).

Magnetic resonance imaging is the preferred imaging modality, which primarily shows bilateral subcortical hyperintense white matter regions, predominantly involving the parietal and occipital lobes. Hyperintensity on diffusion sequences with an elevated Apparent Diffusion Coefficient (ADC) is typically seen on MRI, indicating vasogenic oedema. In contrast, cytotoxic oedema caused by ischaemia is hyperintense and has low diffusion coefficient. The use of magnetic resonance angiography and venography helps rule out alternative diagnoses {Cerebral Venous Sinus Thrombosis (CVST) or stroke} (6).

Although the exact pathogenesis of PRES is unclear, it is thought to be due to rapid increase in blood pressure resulting in dysfunction of the autoregulatory mechanisms of cerebral blood vessels leading to vascular leakage and oedema. It is also suggested that the rapid rise in blood pressure could damage the blood-brain barrier, which explains involvement of the posterior circulation in PRES since it lacks sympathetic tone. However, in patients of PRES associated with other conditions like organ transplants, renal disease, and the use of immunosuppressive drugs with normal blood pressure, there may be certain endogenous or exogenous toxins that cause endothelial damages and vasogenicoedema (7).

Some cases of COVID-19 with PRES may develop macrophage activation syndrome (MAS) with fever and increased levels of tumour Necrosis Factor-alpha (TNF-?). TNF-? increases vascular permeability and upregulates vascular endothelial growth factor in the presence of hypoxemia causing endothelial injury and oedema (8).

The majority of PRES cases however, are associated with hypertension. In a study of six cases of PRES in COVID-19 patients by Colombo A et al., it was reported that CSF-PCR for SARS-CoV-2 genome was negative in all cases and that blood pressure fluctuations were the most relevant factor in PRES pathogenesis (9). In a study of 15 COVID-19 patients with PRES by Hinchey J et al., 12 patients had abrupt increases in blood pressure (1).

Characteristic imaging findings and reversibility of symptoms were diagnostic of PRES. Since, other causes of hypertension were ruled out, and evidence of hypertension associated with COVID-19 is documented, the cause of PRES was determined to be due to hypertension secondary to COVID-19 infection. Elevated cardiac markers with normal electrocardiography and 2D-echocardiography were suggestive of myocardial injury.

The pathophysiology and consequences of COVID-19 are still poorly understood. COVID-19 patients without prior hypertension showed a rise in blood pressure during hospitalisation, and majority of the patients had higher systolic blood pressure. In a study of 190 COVID-19 patients, 8.42% patients had a rise in blood pressure during hospitalization (10). Another study on153 confirmed COVID-19 patients showed new onset hypertension in 18 patients (11).

The binding of SARS-CoV-2 to Angiotensin-Converting Enzyme 2 (ACE2),, which inhibits angiotensin II breakdown and leads to increased blood pressure, is one possible mechanism. Another theory is that excessive Renin-Angiotensin-Aldosterone system (RAS) activation promotes inflammatory response and cytokine storm, which stimulates the Nicotinamide Adenine Dinucleotide Phosphate/Nicotinamide Adenine Dinucleotide Phosphate Hydrogen reduced form (NADP/NADPH) oxidase system and causes cell contraction and vasoconstriction (10).

Angiotensin II has been shown to have direct or indirect effects on cardiomyocytes, some of which were linked to proinflammatory and prohypertrophic responses. Increased Angiotensin II activity could lead to cardiac inflammation, oxidative stress, and myocyte death, especially when the balance between ACE and ACE2 was altered in COVID-19 patients. This hypothesis explains why COVID-19 patient’s blood pressure may rise in parallel with mild cardiac injury (12). Studies have suggested that SARS-CoV-2 binds to ACE2 receptors, which are abundant in myocytes andcan result in direct injury to cardiomyocytes (13). Though the exact mechanism is still unknown, it is becoming evident that RAS plays a major role in hypertension and COVID-19 infection.

Conclusion

Early identification, treatment of symptomatology, and correction of the underlying cause are all important aspects of PRES management. As the term implies, proper treatment is expected to result in a complete recovery. However, there have been reports of long-term complications and fatalities. Recurrence of symptoms has been observed in a few cases.

References

1.
Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996;334(8):494-500. [crossref] [PubMed]
2.
Kumari DS, Arumilli MNLN, Reddy LSK, Reddy DN, Motor R. Acute Intermittent Porphyria Presenting with Posterior Reversible Encephalopathy Syndrome: A Rare Cause of Abdominal Pain and Seizures. Indian J Crit Care Med. 2020;24(8):724-26. [crossref] [PubMed]
3.
Legriel S, Pico F, Azoulay E. Understanding Posterior Reversible Encephalopathy Syndrome. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2011. Annual Update in Intensive Care and Emergency Medicine 2011, vol 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18081-1_56. [crossref]
4.
Bartynski WS. Posterior Reversible Encephalopathy Syndrome, Part 1: Fundamental Imaging and Clinical Features. AJNR Am J Neuroradiol. 2008;29(6):1036-42. [crossref] [PubMed]
5.
Admane SS, Yelne TS, Giri PJ. A Case of Posterior Reversible Encephalopathy Syndrome Mimicking Stroke. Indian J Crit Care Med. 2020;24(9):877-78. [crossref] [PubMed]
6.
Hugonnet E, da Ines D, Boby H, Claise B, Petitcolin V, Lannareix V, et al. Posterior reversible encephalopathy syndrome (PRES): Features on CT and MR imaging. Diagnostic and Interventional Imaging. 2013;94(1):45-52. [crossref] [PubMed]
7.
Alnass AJ, Alamer RA, Alamri HH, Alharthi AA, Assad MA, Sedran MK, et al. Posterior Reversible Encephalopathy Syndrome: A Rare Complication in COVID-19. Cureus. 2021;13(10). [crossref] [PubMed]
8.
Arslan G, Besci T, Karaca Ö, AylanGelen S. Posterior reversible encephalopathy syndrome related to COVID-19 in a child. Pediatrics International. 2022;64(1):e14908. [crossref]
9.
Colombo A, Martinelli Boneschi F, Beretta S, Bresolin N, Versino M, Lorusso L, et al. Posterior reversible encephalopathy syndrome and COVID-19: A series of 6 cases from Lombardy, Italy. eNeurologicalSci. 2021;22:100306. [crossref] [PubMed]
10.
Chen G, Li X, Gong Z, Xia H, Wang Y, Wang X, et al. Hypertension as a sequela in patients of SARS-CoV-2 infection. PLoS ONE. 2021;16(4):e0250815. [crossref] [PubMed]
11.
Akpek M. Does COVID-19 Cause Hypertension? Angiology. 2021;33197211053903. [crossref] [PubMed]
12.
Forrester SJ, Booz GW, Sigmund CD, Coffman TM, Kawai T, Rizzo V, et al. Angiotensin II signal transduction: An update on mechanisms of physiology and pathophysiology. Physiological Reviews. 2018;98(3):1627-738. [crossref] [PubMed]
13.
Khan S, Rasool ST, Ahmed SI. Role of Cardiac Biomarkers in COVID-19: What Recent Investigations Tell Us? Current Problems in Cardiology. 2021;46(10):100842. [crossref] [PubMed]

DOI and Others

DOI: 10.7860/JCDR/2022/56337.16512

Date of Submission: Mar 13, 2022
Date of Peer Review: Apr 05, 2022
Date of Acceptance: Apr 11, 2022
Date of Publishing: Jun 01, 2022

AUTHOR DECLARATION:
• Financial or Other Competing Interests: None
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. Yes

PLAGIARISM CHECKING METHODS:
• Plagiarism X-checker: Mar 23, 2022
• Manual Googling: Apr 15, 2022
• iThenticate Software: May 28, 2022 (25%)

ETYMOLOGY: Author Origin

JCDR is now Monthly and more widely Indexed .
  • Emerging Sources Citation Index (Web of Science, thomsonreuters)
  • Index Copernicus ICV 2017: 134.54
  • Academic Search Complete Database
  • Directory of Open Access Journals (DOAJ)
  • Embase
  • EBSCOhost
  • Google Scholar
  • HINARI Access to Research in Health Programme
  • Indian Science Abstracts (ISA)
  • Journal seek Database
  • Google
  • Popline (reproductive health literature)
  • www.omnimedicalsearch.com