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Case report article, case report: clinical features of a covid-19 patient with cirrhosis.

clinical case study on covid 19

Coronavirus disease 2019 (COVID-19) was first reported in Wuhan, Hubei Province, China in December 2019. At present, COVID-19 has emerged as a global pandemic. The clinical features of this disease are not fully understood, especially the interaction of COVID-19 and preexisting comorbidities and how these together further impair the immune system. In this case study, we report a COVID-19 patient with cirrhosis. A 73-year-old woman with cirrhosis reported a fever and cough on February 6, 2020. CT of the chest indicated an infection in her bilateral lungs. She tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The woman was treated with lopinavir and ritonavir tablets and interferon alpha-2b injection, but there was no obvious effect. Although this patient was basically asymptomatic after 2 days in the hospital, the inflammation of the bilateral lungs was slow to subside as shown in CT of the chest. In addition, the white blood cell count (WBC), absolute neutrophil count, and absolute lymphocyte count remained decreased and the result of real-time reverse transcription polymerase chain reaction (PCR) (rRT-PCR) assay was still positive for SARS-CoV-2 on hospital day 28. After infusion of plasma from a recovered COVID-19 patient four times, the patient tested negative for SARS-CoV-2. She was discharged on March 13, 2020. This patient tested negative for SARS-CoV-2 after infusion of plasma from a recovered COVID-19 patient four times. Cirrhosis could impair the homeostatic role of the liver in the systemic immune response, which may affect the removal of SARS-CoV-2. This could lead to a diminished therapeutic effect of COVID-19. Thus, clinicians should pay more attention to COVID-19 patients with cirrhosis.

Introduction

At present, many studies have indicated the epidemiological and clinical characteristics of coronavirus disease 2019 (COVID-19) ( 1 – 4 ). However, there are many diseases that may affect the immune system, such as AIDS, cirrhosis, and advanced malignant tumors, which may affect the removal of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), further affecting the treatment of COVID-19 patients. A nationwide analysis in China analyzed the major strategies for patients with cancer in this COVID-19 crisis ( 5 ). The process of advanced cirrhosis is complicated with cirrhosis-associated immune dysfunction. Cirrhosis has the potential to injure the homeostatic role of the liver in the immune system ( 6 , 7 ). In this case study, we report a case of a COVID-19 patient with cirrhosis. We describe the symptoms, diagnosis, treatment, and management of this patient, which may provide more information for the treatment of COVID-19 patients with cirrhosis.

Case Report

On February 11, 2020, a 73-year-old woman came to the Fever Clinic of the First Hospital of Changsha, China. Ten minutes later, she was taken to the examination room and evaluated by a clinic doctor. The chief complaint of the patient was a fever—her body temperature peaked at 39°C—with cough, expectoration, shortness of breath, and general weakness that started prior 5 days. She developed mild diarrhea (3–4 stools/day) 2 days prior to coming to the hospital. Her daughter was diagnosed with COVID-19. Given her symptoms and recent close contact with a COVID-19-positive patient, she decided to go to a healthcare provider. The patient had a history of cirrhosis and type 2 diabetes, but no history of smoking or drinking. Physical examination indicated a body temperature of 38.8°C, a pulse of 100 beats/min, a respiratory rate of 22 breaths/min, an oxygen saturation of 85%, and bowel sounds at four times/min. She presented with a characteristic feature of chronic liver disease, hepatic facies, and liver palms, but no spider nevus. In addition, she had thick breathing sounds on both sides of the lungs and audible wet murmurs in both the lungs. The abdomen of the patient was soft and had no lumps. No pain was found in the liver without mobile dullness.

Considering the possibility of SARS-COV-2 infection, we performed a chest CT examination and found bilateral pneumonia ( Figure 1 ). The results of a nucleic acid amplification test (NAAT) for influenza A and B were negative. Her blood tests demonstrated simultaneous reduction of the ternary systems (red blood cells: 2.83 × 10 12 cells/l; peripheral blood hemoglobin: 83 g/l; white blood cells: 0.78 × 10 9 cells/l; lymphocytes: 0.11 × 10 9 cells/l; lym%: 14.5%; platelets: 41 × 10 9 cells/l) and an elevated percentage of neutrophils (0.65 × 10 9 /L; n%: 82.8%), C-reactive protein (62.5 mg/l), and erythrocyte sedimentation rate (129 mm/h) ( Table 1 ). In view of the close contact history and clinical examination results of the patient, we carried out COVID-19 test for the patient. Specimens were collected following the Chinese Center for Disease Control and Prevention (CCDC) guidance. The results showed that she tested positive for SARS-COV-2. Therefore, she was admitted to the isolation ward for further treatment.

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Figure 1 . CT of the chest of the patient. (A) CT of the chest was obtained on February 12, 2020 (hospital day 2, illness day 6). The major morphogenesis of her bilateral lungs took on increased bronchovascular shadows and multiple patchy and maculas shadows, with cord-like ground-glass opacity (GGO) in the middle and lower regions of the lung. CT scan of the chest also showed increased lung markings. The texture of the trachea and blood vessels in both the lungs became thicker. (B) CT of the chest was obtained on February 16, 2020 (hospital day 6, illness day 10). The patchy lesions and maculas in both the lungs were partially absorbed. Increased lung markings were observed in the bilateral lungs. (C) CT of the chest was obtained on February 20, 2020 (hospital day 10, illness day 14). Decreased density of the patchy lesions in both the lungs was observed. The texture of the trachea and blood vessels in both the lungs became thicker. (D) CT of the chest was obtained on February 24, 2020 (hospital day 14, illness day 18). The pulmonary lesions remained unchanged. (E) CT of the chest was obtained on February 28, 2020 (hospital day 18, illness day 22). There was no obvious change in the patchy lesions in both the lungs. GGO was slightly increased. (F) CT of the chest was obtained on March 3, 2020 (hospital day 22, illness day 26). The major lesions of the bilateral lungs were not absorbed. (G) CT of the chest was obtained on March 10, 2020 (hospital day 29, illness day 33). The multiple patchy and maculas shadows of the bilateral lungs were further absorbed and the bronchovascular shadows were reduced.

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Table 1 . Clinical laboratory results.

On day 1 of the hospital stay (illness day 5), the patient was administered lopinavir and ritonavir tablets (2 pills BID peros), which were recommended by the Diagnosis and Treatment of Pneumonitis with COVID-19 Infection (DTPI) published by the National Health Commission of the People's Republic of China (PRC) and interferon alpha-2b injection (5 million IU added into 2 ml of sterile water, inhalation BID). To inhibit inflammation in the lungs, she was treated with methylprednisolone sodium succinate (40 mg QD, intravenously). Yellow-green expectoration predicted the presence of a bacterial infection and, as such, moxifloxacin hydrochloride and sodium chloride injection (0.4 g QD) were given intravenously to the patient as treatment. Moreover, other supportive treatments included human immunoglobulin (10 g QD, intravenously) for improving immunity, Bifidobacterium lactobacillus trifecta orally for regulating the intestinal flora, recombinant human granulocyte colony-stimulating factor for promoting cell proliferation, and ampeptide elemente tablets for promoting the formation of platelets.

On day 2 of the hospital stay (illness day 6), she was asymptomatic apart from a cough, expectoration, chest tightness, and shortness of breath. Additionally, her temperature dropped to 36.9°C, but she reported that diarrhea still existed, approximately four times/day ( Table 2 ). CT scans showed that the patchy infiltration was scattered as a small range of ground-glass opacity effusion and strip lesions in the bilateral lungs, which was similar to day 1 in the hospital ( Figure 1 ). Otherwise, the laboratory results reflected that there was still a reduction in the tertiary system and hypoproteinemia due to liver dysfunction. Human serum albumin (50 ml BID) was then given intravenously. To prevent of episodes of hepatic encephalopathy, which is a chronically debilitating complication of hepatic cirrhosis, lactulose was added to the therapeutic regimen of the patient and nutritious meals were supplied to improve her anemia. The CCDC repeatedly confirmed that the oropharyngeal swabs of this patient tested positive for SARS-CoV-2 by real-time reverse transcription PCR (rRT-PCR) assay.

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Table 2 . Body temperatures and symptoms from February 6 to March 13, 2020.

On day 3 of the hospital stay (illness day 7), the patient reported she felt better. Her pulse oxygen saturation increased significantly, up to 100%, at an oxygen flow rate of 2 l/min. Since that she still had diarrhea symptoms and lactulose was stopped to avoid the occurrence of imbalance of water and electrolytes. On day 4 of her hospital stay (illness day 8), a gastroenterologist was contacted to evaluate the persistent diarrhea of the patient. According to the suggestion of the gastroenterologist, the patient was treated with pantoprazole enteric-coated tablets (40 mg QD orally) for acid suppression. In addition, reduced glutathione (0.6 g QD) was given intravenously to protect her liver from subsequent damage.

On days 5–10 of the hospital day (illness days 9–14), the patient reported that her diarrhea improved to a degree and her clinical condition improved with supportive care. On hospital day 6 of the hospital stay, CT scans showed that the partial patchy lesions in the bilateral lungs were absorbed compared with the CT images obtained previously ( Figure 1 ). Given the clinical presentation of the patient, treatment with human serum albumin was stopped on day 6 of the hospital stay. Lopinavir and ritonavir tablets, methylprednisolone sodium succinate, moxifloxacin, ampeptide elemente tablets, pantoprazole enteric-coated tablets, and human immunoglobulin were stopped on day 8 of the hospital stay of the patient ( Table 3 ). However, the clinical course of the patient continued to deteriorate in terms of her respiratory symptoms, who typically presented with a cough and shortness of breath. Thymosin (0.1 g QD) and plasma (200 ml) from recovered COVID-19 patients plasma were then given intravenously to boost the immunity of the patient. On day 9 of the hospital stay (illness day 13), the C-reactive protein of this patient dropped to 3.4 mg/l. Nevertheless, CT scans of the chest indicated that the symptoms of the bilateral lungs of the patient did not improve on day 10 of the hospital stay ( Figure 1 ). Moreover, the oropharyngeal swabs of this patient retested positive. Therefore, chloroquine phosphate (0.5 g BID) was administered orally instead. Additionally, the treatments did not improve the level of blood cells because of liver dysfunction and hypersplenism caused by cirrhosis.

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Table 3 . Order sheet of the physician.

On days 11–18 of the hospital stay (illness days 15–22), she was in good clinical condition, except for a persistent cough and intermittent diarrhea. In order to further alleviate the diarrhea of the patient, montmorillonite powder (3 g QD) and loperamide hydrochloride (2 mg QD) were administrated orally. Moreover, interferon alpha-2b injections were stopped due to its limited effect on the clearance of the virus and the plasma from recovered COVID-19 patients was infused again on day 15 of the hospital stay (illness day 19). As the diarrhea of the patient improved, antidiarrheal drugs were discontinued on day 18 of the hospital stay (illness day 22).

On days 19–29 of the hospital stay (illness days 23–33), the vital signs of the patient were largely stable. The patient reported that her cough and diarrhea had abated and her clinical condition improved. Given these good clinical conditions, a reduction in glutathione injections was initiated on day 19 of her hospital stay. However, since the oropharyngeal swabs of this patient tested positive again, she was treated with plasma from a recovered COVID-19 patient for the third time. On day 29 of the hospital stay (illness day 33), CT scans showed that the patchy lesions in the bilateral lungs of the patient had absorbed compared with the CT images obtained previously ( Figure 1 ). On the same day, the patient tested negative for COVID-19 infection ( Table 1 ). On day 30 of the hospital stay (illness day 34), the patient was once again treated with the plasma from a recovered COVID-19 patient in order to ensure that the virus was completely cleared. On days 30–31 of the hospital stay, the patient tested negative for COVID-19 by an rRT-PCR assay for two times. She was discharged on March 13, 2020 (day 32 of the hospital stay, illness day 36).

Cirrhosis affects the cellular and humoral immune response of the entire body and the immune system of the liver ( 6 , 8 ). The proportion of CD4 + /CD8 + cells in the liver of patients with cirrhosis decreases and the distribution of lymphocytes varies within different lesions. CD8 + cells predominate in the necrotic area, while CD4 + cells increase in the manifold area. T-helper type 1 (Th1) cells dominate during the early stages of cirrhosis and then gradually drift toward Th2 cells. In order to understand the impact of cirrhosis on the treatment of COVID-19, we report the symptoms, diagnosis, treatment, and management of a COVID-19 patient with cirrhosis.

In this case study, the patient tested positive for SARS-CoV-2, which was supported by CT scan of the chest and she was admitted to the isolation ward at the First Hospital of Changsha City, China. Lopinavir and ritonavir tablets combined with interferon alpha-2b injections were given to her on her first day in the hospital. Though she was basically asymptomatic on day 2 of her hospital stay and her body temperature also returned to a normal range, the inflammation of her bilateral lungs was difficult to subside, suggesting that clinicians should be aware of COVID-19 patients with diseases affecting the immune system. These patients may show mild or even no symptoms, while the inflammation of lungs may be progressing. Therefore, if a person with basic diseases that impair the immune system was exposed to confirmed COVID-19 cases, they should immediately come to the hospital even if they have no symptoms. Also, doctors need to be aware of the progression of inflammation in the lungs.

Previous reports showed that COVID-19 patients with cirrhosis had lower albumin than patients with COVID-19 ( 9 ), which was consistent with the results of this case study. Moreover, Qi et al. discovered that leukopenia, lymphopenia, and thrombocytopenia occurred in COVID-19 patients with cirrhosis ( 10 ), which were similar to the results we obtained. Additionally, increasing evidence indicated that patients with COVID-19 exhibited a hypercoagulability in the lung ( 11 ). In this case study, the D-dimers of COVID-19 patient with cirrhosis were elevated, suggesting hypercoagulability of the patient. The liver synthesizes a variety of coagulation factors. When cirrhosis causes liver insufficiency, the production of coagulation factors is reduced, which leads to prolonged prothrombin time (PT), activated partial thromboplastin time (APTT) and thrombin time (TT), and a decrease of fibrinogen. Therefore, the PT, APTT, and TT of COVID-19 patient with cirrhosis were prolonged and fibrinogen was decreased, which was similar to the previous study ( 12 ). In addition, venous thromboembolism (VTE) including deep venous thrombosis (DVT) is common in cirrohsis patients. Additionally, the patient in this case study was treated with antiviral drugs, which had no obvious effect on her symptoms. Previous study indicated that 96% cirrhotic patients with confirmed SARS-CoV-2 infection needed hospitalization or prolonged an ongoing one ( 13 ). In this case study, we observed similar results. This COVID-19 patient with cirrhosis was hospitalized for 32 days. She was tested positive for COVID-19 on day 25 of her hospital stay. Moreover, the numbers of WBC and the absolute neutrophil count and absolute lymphocyte count remained reduced in this patient. The process of advanced cirrhosis is complicated with cirrhosis-associated immune dysfunction. Cirrhosis has the potential to injure the homeostatic role of the liver in the immune system, which may be associated with the process of COVID-19. Additionally, although the mortality of COVID-19 was mediated by pulmonary involvement, cirrhosis is assumed to be a high-risk factor for severe COVID-19 because of an altered gut-liver axis and inherent immune dysfunction. Cirrhosis can impair the cellular and humoral immune system of the entire body, which may impair the removal of SARS-CoV-2. Thus, physicians may need to monitor immune indicators in COVID-19-positive patients with comorbidities that impair the immune system.

The patient in this case study was administered the plasma (200 ml) from recovered COVID-19 patients four times. After the last administration of plasma on day 30 of the hospital stay, the patient tested negative for SARS-CoV-2 three consecutive times and then she was discharged on day 32 of her hospital stay. This suggested that the treatment for COVID-19 is passive immunotherapy. Cirrhosis can impair the homeostatic role of the liver in the systemic immune response; thus, passive immunotherapy, such as plasma administration from recovered COVID-19 patients, may be an option for treatment. However, this case study has a limitation that needs to be cautious. These findings have only been observed in one patient. Further multicenter with large sample studies are needed to perform to verify the results.

This case study described the symptoms, diagnosis, treatment, and management of a COVID-19 patient with cirrhosis, emphasizing the need to pay attention to underlying diseases in COVID-19-positive patients. More information about this disease is still needed in order to successfully explore its clinical management.

Data Availability Statement

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Ethics Statement

The studies involving human participants were reviewed and approved by The First Hospital of Changsha City Committee for Clinical Research. The patients/participants provided their written informed consent to participate in this study. Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.

Author Contributions

JZ and JS conceived and designed the study and also critically revised the manuscript. JZ and WW conducted the experiments and drafted the manuscript. DJ, KH, FZ, YX, and ZZ contributed to the revision of the manuscript. All authors have read and approved the final manuscript.

This study was funded by the Innovative Major Emergency Project Funding against the New Coronavirus Pneumonia in Hunan Province (Grant Nos. 2020SK3014 and 2020SK3013), the Key Research & Developmental Program of Hunan Province (2022SK2047), Chinese Public Health Union (GWLM202039), Health and Family Planning Commission Fund Project in Hunan Province (Grant No. B2017209), Natural Science Foundation of Hunan Province (Grant No. 2018JJ2452), New Coronavirus Pneumonia Emergency Project of Changsha Science and Technology Bureau (Grant Nos. kq2001010 and kq2001008), the Mittal Innovation Project of Central South University (Grant No. GCX20190879Y) and the Fundamental Research Funds for the Central Universities of Central South University (Grant No. 2018zzts930). The study funders/sponsors had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher's Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Acknowledgments

The authors would like to thank all the co-investigators and colleagues who made this study possible. The authors would like to thank the Changsha CDC, Hunan CDC, and CCDC for their assistance with laboratory testing. We thank LetPub ( www.letpub.com ) for its linguistic assistance during the preparation of this revised manuscript.

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Keywords: COVID-19, cirrhosis, SARS-CoV-2, treatment, cured patient

Citation: Zhou J, Jiang D, Wang W, Huang K, Zheng F, Xie Y, Zhou Z and Sun J (2021) Case Report: Clinical Features of a COVID-19 Patient With Cirrhosis. Front. Med. 8:678227. doi: 10.3389/fmed.2021.678227

Received: 09 March 2021; Accepted: 01 November 2021; Published: 26 November 2021.

Reviewed by:

Copyright © 2021 Zhou, Jiang, Wang, Huang, Zheng, Xie, Zhou and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Zhiguo Zhou, cszhouzhiguo@outlook.com ; Jingjing Sun, 2520064@zju.edu.cn

† These authors have contributed equally to this work

This article is part of the Research Topic

COVID-19 and the Digestive System

Novel coronavirus 2019 (COVID-19): A case report and review of treatments : Medicine

clinical case study on covid 19

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Novel coronavirus 2019 (COVID-19)

A case report and review of treatments.

Editor(s): Saranathan., Maya

a Department of Medicine, Hackensack Meridian Jersey Shore University Medical Center Neptune

b Department of Medicine, Hackensack Meridian School of Medicine at Seton Hall University Nutley

c Department of Pulmonology and Critical Care, Hackensack Meridian Jersey Shore University Medical Center Neptune, NJ, USA.

∗Correspondence: Steven Douedi, Jersey Shore University Medical Center, Neptune, NJ 07753 (e-mail: [email protected] ).

Abbreviations: ARDS = acute respiratory distress syndrome, CoV = coronavirus, COVID-19 = novel coronavirus 2019, CVVHD = continuous veno-venous hemodialysis, ED = emergency department, FiO2 = fraction of inspired oxygen, ICU = intensive care unit, MERS-CoV = Middle East respiratory syndrome coronavirus, PCR = polymerase chain reaction, PEEP = positive end-expiratory pressure, RSV = Respiratory syncytial virus, SARS-CoV = severe acute respiratory syndrome coronavirus, SARS-CoV-2 = severe acute respiratory syndrome coronavirus 2 .

How to cite this article: Douedi S, Miskoff J. Novel coronavirus 2019 (COVID-19): a case report and review of treatments. Medicine . 2020;99:19(e20207).

The authors have no conflicts of interests to disclose.

This manuscript is a unique submission and is not being considered for publication by any other source in any medium. Further, the manuscript has not been published, in part or in full, in any form.

The patient's next of kin provided consent for this manuscript to be published.

Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.

This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

Rationale: 

Novel coronavirus 2019 (COVID-19) also known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped, non-segmented positive-sense RNA virus belonging to the beta-coronaviridae family. This virus is known to cause severe bilateral pneumonia and acute respiratory distress syndrome (ARDS) which can lead to difficulty breathing requiring mechanical ventilation and intensive care unit management.

Patient concerns: 

A 77-year-old female with a history of hypertension and hyperlipidemia who presented as a transfer to our hospital facility with worsening fevers, cough, and respiratory distress.

Diagnosis: 

Chest X-rays revealed bilateral infiltrates worse at the lung bases and CT scan of the chest showed bilateral ground-glass opacities consistent with COVID-19. While our testing revealed a negative COVID-19 result at our institution, the result at a previous hospital returned a positive result.

Interventions: 

She was being treated aggressively in the intensive care unit with high dose intravenous ascorbic acid, hydroxychloroquine, and anti-interleukin-6 monoclonal antibody. She also received a loading dose of remdesivir however was unable to complete the course due to organ failure and requirement of vasopressors for hemodynamic stability.

Outcomes: 

She remained critically ill and was eventually placed on comfort care as per the family's wishes and passed away.

Lessons: 

With a rapidly growing death rate and more than 200,000 confirmed cases worldwide, COVID-19 has become a global pandemic and major hit to our healthcare systems. While several companies have already begun vaccine trials and healthcare facilities have been using a wide-range of medications to treat the virus and symptoms, there is not yet an approved medication regimen for COVID-19 infections. The alarming increase in cases per day adds additional pressure to find a cure and decrease the global health burden and mortality rate.

1 Introduction

The novel coronavirus 2019 (COVID-19) also known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an enveloped, non-segmented positive-sense RNA virus belonging to the beta-coronaviridae family. [1] COVID-19 has been found to be the cause of severe pneumonia and acute respiratory distress syndrome (ARDS) with a significantly high mortality rate. [2] According to the World Health Organization, there are 207,855 confirmed cases and 8648 deaths from COVID-19 as of March 19, 2020 and rapidly increasing. [3] Originating from bats like other virulent coronavirus (CoV) strains such as severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), COVID-19 has become the focus of the medical world and the pandemic of 2020. [1,4] We present a case of elderly female presenting with fever, cough, and shortness of breath found to be positive for COVID-19 and started on high-dose IV ascorbic acid, anti-interleukin-6, hydroxychloroquine, and remdesivir requiring high ventilator settings and eventually requiring vasopressors and continuous veno-venous hemodialysis (CVVHD).

2 Case presentation

A 77-year-old Middle-Eastern female with a medical history of hypertension and hyperlipidemia presented to the emergency department (ED) from a day care facility apartment where 2 people at the facility have tested positive for COVID-19 but she did not have any direct contact with these individuals. About 5 days before admission the patient developed a fever with a temperature of 102°F at home, and went to her primary medical doctor who sent her to the ED. In the ED she was found to have bilateral opacities on chest X-ray and had continued intermittent fevers with generalized weakness, cough, lethargy, and dyspnea and was sent for testing for COVID-19 then transferred to our facility for further management. In our facility, her temperature was 101.7°F, blood pressure 148/76 mm Hg, heart rate of 99 beats per minute, respiratory rate of 18 per minute, and oxygen saturation of 93% on room air. Physical exam was significant for a dry cough and bilateral rales on auscultation of the lung fields bilaterally but was unremarkable otherwise. A chest X-ray ( Fig. 1 ) was performed showing bilateral opacities throughout the lung fields with predominance of the lower lung lobes she was admitted for possible pneumonia with isolation precautions for suspected COVID-19 and was started on oxygen via nasal cannula and on 1-gram ceftazidime intravenously every 8 hours and 500 mg azithromycin orally daily. CT scan of the chest ( Fig. 2 ) was performed showing bilateral ground glass appearance throughout the lung with predominance in the peripheral lower lobes. Respiratory viral panel was sent including a repeat COVID-19 test ( Table 1 ). All results came back negative however the patient's condition deteriorated 2 days after admission to our facility, and she became hypoxic to 85% oxygen saturation while on nasal cannula and remained spiking fevers up to 103.4°F. She was intubated and transferred to the intensive care unit (ICU) for further management and was switched to ceftriaxone 1 g intravenously daily and azithromycin 500 mg via orogastric tube daily and was started on hydroxychloroquine 400 mg loading dose followed by 200 mg twice daily for a 7-day course. She required 100% fraction of inspired oxygen (FiO2) and a positive end-expiratory pressure (PEEP) of 12 to maintain an oxygen saturation of >90%. 12 hours later, the COVID-19 test from the initial facility returned positive results. On day 3 of hospitalization she was started on 6 g of IV ascorbic acid twice daily and given one dose of 8 mg per kg (567 mg) of tocilizumab, an anti-interleukin-6 monoclonal antibody. Due to a shortage of vitamin C in the hospital, her dose was decreased to 1 g IV daily on the 6th day of hospitalization and she was given another dose of tocilizumab. On day 7, her PEEP increased from 12 to 16 due to worsening oxygen saturation and increased requirement despite 100% FiO2. Due to severe ARDS, the decision was made to prone the patient for 18 hours a day. She completed her course of antibiotics and hydroxychloroquine but remained on vitamin C and zinc. Approval for remdesivir was obtained from Gilead Sciences Inc and she was given a loading dose of 200 mg on day 10 and due to worsening oxygen saturation her PEEP was again increased to 18. On day 11, the patient was unable to tolerate being prone due to significant desaturation to 65% on pulse oximetry and remained supine. She eventually required levophed for maintenance of hemodynamic stability and her creatinine increased from her baseline of 0.5-0.6 since admission until day 10 to 2.65 on day 12. For this reason, remdesivir was discontinued and nephrology was consulted and recommended CVVHD on day 13. On day 14 her PEEP requirement again increased to 20 while on 100% FiO2 to maintain an oxygen saturation >90%. Her condition remained critical while being aggressively managed in the ICU and ultimately the patient's family decision was to pursue comfort measures and the patient passed away.

F1

3 Discussion

COVID-19 is the cause of severe viral pneumonia rapidly leading to ARDS. In a case series of 135 patients, Wan et al reported 88.9% of patients presented with a fever and 76.5% had a cough. [5] Fatigue and myalgias (32.5%), headache (17.7%), and dyspnea (13.3%) were less commonly reported. [5] These symptoms were also found on presentation with our patient. While the COVID-19 tests were pending, the CT scan of the chest provided valuable information as it met the trend of findings in infected patients. Wan et al obtained CT scans on all patients in their study and found bilateral involvement and multiple patchy or ground glass appearance to be the primary finding. [5] Huang et al found similar findings where 98% of CT scans obtained had bilateral involvement and multilobular consolidations. [6] These findings on CT scans are not unusual for a viral pneumonia. Influenza A (H1N1) was first found to cause a pandemic in 2009, a retrospective review of 92 patients by Çörtük et al found 69.6% of patients with H1N1 had bilateral patchy pneumonic infiltrates and 41.3% had bilateral ground glass opacities. [7] While the lack of rapid testing for COVID-19 has caused a delay in diagnosis, perhaps the use of CT scans could provide an increased suspicion of COVID-19 infection leading to earlier treatment and management.

Our patient presented in this case received treatment with vitamin C and zinc, both of which are known to improve the human immune system and aid in shortening the duration of and improving outcomes in respiratory infections including pneumonia. [8,9] In addition to vitamin and mineral supplements, hydroxychloroquine and azithromycin have obtained a large amount of attention for the treatment of COVID-19. Hydroxychloroquine, a well-known anti-malarial and auto-immune medication, is relatively inexpensive and has been extensively studied in the treatment for COVID-19. Studies have suggested hydroxychloroquine can interfere with glycosylation of the coronavirus receptors and increase endosomal pH thus inhibiting viral fusion and decreasing viral load. [10,11] Gautret et al reported a synergistic effect using hydroxychloroquine and azithromycin in viral elimination and decreasing viral load. [12] Despite this evidence, the use of hydroxychloroquine for viral infections has been questioned. Roques et al reported a study using chloroquine in Chikungunya virus reporting cytokines were reduced causing the adaptive immune response to be delayed, exacerbating fever, and unchanged suppression of viral load. [13] While further studies are in need to provide concrete evidence on the use of hydroxychloroquine, clinical trials from China have already shown promising results for COVID-19 and several countries around the world have begun using these medications. Tocilizumab, a recombinant humanized anti-interleukin-6 receptor monoclonal antibody, has been extensively used in auto-immune conditions such as rheumatoid arthritis. [14] With this monoclonal antibody, interleukin-6 function is blocked and hence the differentiation of T helper cells and B cells into immunoglobulin-secreting cells are inhibited. [14] The cytokine storm observed in patients with COVID-19 has been difficult to control and manage leading to increased mortality, tocilizumab therefore helps decrease the immune response and the resulting damage caused by cytokines. [6,15] While still not approved in the United States, tocilizumab has thus far shown promising results in clinical trials. [15]

Other treatments for COVID-19 have also emerged and have thus far shown promising results in ongoing clinical trials. Of these, remdesivir (GS-5734) and favipiravir (T-705) have become the center of attention. Remdesivir is an adenosine analog that incorporates into viral RNA causing premature termination. [10,14] It has been found effective at inhibiting viral replication in Ebola, SARS-CoV, and MERS-CoV infections. [10,16,17] Favipiravir, an RNA-dependent RNA polymerase inhibitor, has already obtained approval for the treatment of COVID-19 in China on February 15th, 2020. [18] Studies have shown favipiravir inhibited RNA polymerase activity and thus prevented replication of RNA viruses like COVID-19 with minimal side effects. [18] Remdesivir (GS-5734, Gilead Sciences Inc.) is currently under several clinical trials and all of its side effects have not yet been defined. In our patient, within 2 days of starting remdesivir our patient had worsening renal function eventually requiring CVVHD and vasopressors thus preventing further treatment with the medication. While our patient was critically ill in the ICU, it is not known if this medication was the cause for further decompensation due to kidney injury. Further studies and clinical trials are required to fully understand the role of remdesivir and other medications in COVID-19 infected patients.

4 Conclusion

COVID-19 is a serious infection that has led to thousands of cases of severe pneumonia, ARDS, and even deaths across the globe. As of now there are no approved treatments for this viral pandemic. While several medications have shown to be effective in clinical trials, further studies are needed to establish dosing, treatment course, and side effects of these medications. As the number of cases and deaths continue to increase in the world, the race to develop faster testing modalities to rapidly diagnose and manage these patients earlier continues to be the focus of the global healthcare system.

Author contributions

Conceptualization: Steven Douedi, Jeffery Miskoff.

Writing – original draft: Steven Douedi.

Writing – review & editing: Steven Douedi, Jeffery Miskoff.

acute respiratory distress syndrome; coronavirus; novel coronavirus 2019; infection; respiratory; severe acute respiratory syndrome coronavirus 2

COVID-19: AAPA 2021 Case Studies

clinical case study on covid 19

Although research on SARS-CoV-2 virus has exploded since it first appeared in Wuhan, China in late 2019, much remains unknown about the virus, including some of the rarer clinical signs, symptoms, and outcomes. Novel presentations of COVID-19 disease and atypical clinical outcomes were shared at the American Academy of PAs 2021 Conference (AAPA 2021).

A selection of these cases, including patients with acute hepatitis, peripheral ischemia, and bilateral pulmonary embolism, are summarized below.

Case 1: Acute Hepatitis in COVID-19

Acute hepatitis may be just one of many atypical COVID-19 manifestations. Approximately 44% of patients with the disease have liver function test abnormalities, but the mechanism behind how the virus impacts the liver is still unknown, explained Elliston Whitley, MA, MPAS, PA-C, of Mayo Clinic in Arizona. 1

A 25-year-old woman presents to the hospital complaining of abdominal pain, nausea, vomiting, and diarrhea, following a COVID-19 diagnosis 9 days prior. The patient reports minor respiratory complaints that resolved before presentation. The patient has not received treatment for COVID-19, according to the study author.

The diagnostic workup is notable for transaminitis: alanine aminotransferase (ALT) is 420 U/L and aspartate transaminase (AST) is 276 U/L; bilirubin is normal.

Per hepatology consultation, the patient receives an autoimmune panel, viral hepatitis panel, and liver ultrasound with Doppler in order to rule out thrombus. All panels and the ultrasound are negative.

Despite these results, the patient reports persistent gastrointestinal complaints and transaminitis continues to increase, with peak ALT and AST levels of 1069 U/L and 527 U/L, respectively.

The patient undergoes a liver biopsy that reveals mild acute hepatitis , mild macrovesicular steatosis, and mild zone 3 sinusoidal dilation, all of which could be related to her COVID-19 diagnosis, according to the study author.

The patient is ultimately discharged from the hospital with hepatology follow-up.

This case demonstrates that although elevated liver function test results may be common in patients hospitalized with COVID-19, clinicians should not assume that these findings are a direct manifestation of COVID-19. In this case, the patient’s autoimmune and viral pathogen panel were negative, including results for antinuclear antibodies, smooth muscle antibodies, and mitochondrial antibodies, as well as hepatitis A, B, C, and E viruses, Epstein-Barr virus, herpes simplex virus, and cytomegalovirus serologies. Toxicology evaluations also showed undetectable levels of acetaminophen, negative urine drug screen, and negative ethyl glucuronide. Additionally, liver ultrasound showed normal hepatic parenchyma, no dilation of the bile duct, and patent portal and hepatic veins.

Hemochromatosis and alpha-1 antitrypsin deficiency were also ruled out.

A multifactorial treatment approach for this patient included clinicians from internal medicine, infectious disease, and hepatology. Ultimately, the patient was managed through supportive treatment, which included intravenous hydration and antiemetics. At outpatient follow-up evaluation, the patient showed gradual improvement in liver function tests and a full recovery.

“According to current research, liver biopsy findings consistent with hepatocellular injury secondary to COVID-19 frequently include findings of macrovesicular steatosis, mild acute hepatitis, and mild portal inflammation with lymphocytic infiltration,” the presenter noted. These histologic findings and abnormalities in liver function tests are likely due to viral-mediated cytopathic effects, the study author concluded.

Audience members commented that they have seen similar cases, including one in which a patient had prolonged diarrheal symptoms resembling irritable bowel syndrome for months after normalization of liver enzymes in patients with COVID-19 disease.

Case 2: Peripheral Ischemia in COVID-19

It is well known that the SARS-CoV-2 virus binds to the angiotensin-2 receptor to enter target cells. This binding activates the renin-angiotensin system and leads to an increase in angiotensin II. This potent vasoconstrictor increases hypercoagulability and may induce a prothrombotic state — a newly-identified complication of COVID-19, according to Alexis Richards, MPAS, PA-C, and Adrijana Anderson, MMS, PA-C, of Mayo Clinic, Phoenix, Arizona. 2  

In this case, a 38-year-old man presents to the emergency department with pain and darkening of skin on the fifth toe of his left foot, which started 2 days prior and has progressively worsened. At an outside hospital, he undergoes an ultrasound of the foot, which shows no hemodynamically significant stenosis. Results of a computed tomography angiography (CTA) of the abdominal aorta and lower extremity runoff demonstrate a thrombus in the left common iliac artery, extending slightly into the left external iliac artery.

The patient is given a heparin drip and transferred to the Mayo Clinic. The patient denies shortness of breath, fever, or gastrointestinal symptoms, and he tests positive for COVID-19 on rapid swab testing.

He has no prior or family history of either blood clots or pulmonary embolism. Complete blood count shows elevated levels of hemoglobin (18.6 g/dL) and hematocrit (58.1%). D-dimer is also elevated at 0.726 µg/mL.

Due to the arterial thrombus demonstrated on CTA, it is determined that his toe discoloration is due to a microvascular embolic event.

The presenters noted that the patient previously received multiple phlebotomy treatments secondary to an elevated hematocrit, which was thought to be related to testosterone use but may have been related to the patient’s ischemic presentation. The patient’s hemoglobin and hematocrit both improve with fluids (16.6 g/dL and 52.3%, respectively).

The patient is evaluated for vascular surgery but is considered high risk for surgical intervention given his COVID-19 infection and is continued on heparin drip. After symptomatic improvement, the patient is discharged on 3 months of anticoagulation therapy.  

“Given the known hypercoagulability associated with COVID-19, it is probable that [the patient’s] infection precipitated this event,” the presenters wrote, adding that the patient was lost to follow-up.

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Case Study: COVID-19 Management in Patients With Hematologic Malignancies

A 60-year-old man presented to the hospital with five days of fever, dry cough, and shortness of breath. Six years prior, he was diagnosed with κ light-chain multiple myeloma (MM), for which he received induction therapy with cyclophosphamide, bortezomib, and dexamethasone followed by high-dose melphalan and autologous hematopoietic cell transplantation. At the time of admission, he was on maintenance therapy with 10 mg lenalidomide on days 1 to 21 of 28 days, and dexamethasone with no evidence of disease. His vital signs showed a body temperature of 102.9°F, heart rate of 110 bpm, blood pressure at 131/74 mm Hg, respiratory rate of 41, and oxygen saturation of 94 percent at 4 L/min via nasal cannula.

The patient appeared diaphoretic and in acute respiratory distress, with rapid, shallow breathing. Diffuse inspiratory crackles were audible throughout the bilateral lung fields. Empiric broad-spectrum antibiotics were initiated, and the patient was admitted to the special pathogens unit. Within 12 hours after admission, the patient developed increased respiratory distress, and rapidly escalating oxygen requirements prompted his transfer to the intensive care unit (ICU). Upon arrival to the ICU, he was intubated for hypoxemic respiratory failure due to severe ARDS.

Lab results at presentation are shown in the Table. A chest X-ray on admission showed low lung volumes and bilateral atelectasis. Urinary antigens for Streptococcus pneumoniae and Legionella pneumophilia were negative. A polymerase chain reaction (PCR) –based respiratory viral panel was negative for influenza A/B, respiratory syncytial virus, adenovirus, human metapneumovirus, and parainfluenza 1-4. Nasopharyngeal reverse transcription-PCR for SARS-CoV-2 was positive, confirming the diagnosis of COVID-19 pneumonia. The patient was treated with hydroxychloroquine but showed no change in his clinical status. Given the patient’s elevated and rising serum interleukin (IL-6) level, C-reactive protein, and D-dimer, tocilizumab was administered with no appreciable clinical improvement. He was subsequently enrolled on a randomized clinical trial of remdesivir when it became available at our site. After two weeks of mechanical ventilation, the patient was successfully extubated and continues to clinically improve. 

Question 1: Is this patient’s presentation and clinical course typical of COVID-19 pneumonia?

Yes. This case highlights several aspects of COVID-19 pneumonia that have been reported to date. Increasing age, immunosuppression, and medical comorbidities are poor prognostic factors for morbidity and mortality from SARS-CoV-2 infection. 1 This is particularly relevant for our patient with MM on lenalidomide and dexamethasone. It is not known precisely when our patient contracted the SARS-CoV-2 virus. However, a family member of the patient experienced a respiratory illness the week before the patient developed symptoms. This timeline is consistent with the reported median time of five days from initial SARS-CoV-2 infection to symptom onset. 2 Hallmark symptoms of SARS-CoV-2 infection include fever, sore throat, cough (typically nonproductive), shortness of breath, myalgias, and anosmia. 1-4 Importantly, the contribution of asymptomatic SARS-CoV-2 carriers to disease spread is increasingly recognized. 3 Lymphopenia is a nearly universal finding in severely symptomatic patients. Additionally, markers of inflammation, including C-reactive protein, D-dimer, and IL-6, are often elevated in the setting of COVID-19 and may portend less favorable clinical outcomes. Mild elevation in liver transaminases has also been reported. 4 At our institution, we have observed concomitant infections (viral, bacterial, and fungal) in some oncology patients with COVID-19; therefore, a complete infectious disease workup should be considered, especially in high-risk patients, even when COVID-19 is highly suspected or confirmed.

Unfortunately, our patient’s hypoxemic respiratory failure is also characteristic of severe COVID-19, with many patients experiencing rapid clinic deterioration and ultimately requiring invasive mechanical ventilation. 4 To avoid aerosolization of viral particles, we avoid high-flow nasal cannula and noninvasive ventilation modalities. Preliminary experience suggests that early, controlled intubation decreases the risk of virus aerosolization and may improve clinical outcomes, although this is controversial. The most common radiographic findings are bilateral reticular nodular infiltrates and ground glass opacities 2,4 ; however, a proportion of patients may have normal plain film chest radiograph findings at the time of presentation. Chest computed tomography frequently demonstrates diffuse interstitial infiltrates in patients with known infection even if chest x-ray is unremarkable. Prolonged mechanical ventilation is necessary for many patients to recover and associated with a high in-hospital mortality rate. Renal failure requiring renal replacement therapies is a common complication in patients critically ill with COVID-19. Additionally, cardiomyopathy and fatal cardiac arrhythmias have been observed in patients with COVID-19 and warrant close clinical monitoring. 4,5

Question: What testing modalities are clinically available for COVID-19 testing?

Currently, SARS-CoV-2 infection is diagnosed by RT-PCR from nasopharyngeal swab or other respiratory secretions (e.g., tracheal aspirate). In terms of assay performance, the specificity of PCR testing is quite high (99%), with a moderate sensitivity that varies across platforms (80-95%). Consequently, at our institution we recommend two separate tests at least 12 hours apart to confidently rule out SARS-CoV infection in symptomatic hospitalized patients. With improvements in test availability and multiplex capacity, test turnaround time continues to decrease but often depends on where the sample is analyzed (e.g., state reference, commercial, or hospital-based labs). Newer point-of-care testing may soon provide results within minutes; however, the sensitivity has been consistently lower than for laboratory-based techniques. Serologic testing for IgG and IgM antibodies against SARS-CoV-2 have recently been approved by the U.S. Food and Drug Administration (FDA), though few tests have been validated, and there is no evidence of association of antibody levels with clinically relevant immunity. This testing modality can determine if a person has been exposed to the virus and will be helpful for contact tracing, assessing asymptomatic carriers, and measuring efficacy of future SARS-CoV-2 vaccines. Much remains unknown about testing. If there is enough clinical suspicion for COVID-19 infection despite negative PCR assays, our practice is to send serologies and manage patients as if they have infection.

Question: Can you tell us about the investigational COVID-19 therapies this patient received?

Yes. Hydroxycholoroquine has been used for decades to treat malaria and rheumatologic disorders. In a small study from China, hydroxychloroquine was reported to improve the time to symptom resolution in patients with COVID-19. As a result, the FDA has granted Emergency Use Authorization for hydroxycholorquine for patients with COVID-19. However, more recent data demonstrating a lack of clinical benefit of the combination of hydroxycholorquine and azithromycin, combined with prolonged QTc, underscore the need for additional prospective safety and efficacy data. 7 A recent trial of lopinavir-ritonavir in patients with severe COVID-19 did not show a significant clinical benefit. 8 Remdesivir, an adenosine analogue that inhibits viral RNA polymerase, has shown promising in vitro antiviral activity. 9,10 Based on these data, multiple clinical trials of remdesivir alone or in combination with other agents are ongoing. 11 Lastly, IL-6, among other cytokines, are often elevated in severe COVID-19 infection and monoclonal antibodies that block IL-6 signaling (i.e., tociluzumab, siltuximab, sarilumab) may be effective in mitigating the overly exuberant inflammatory response in patients with severe COVID-19. While our patient did not respond to tocilizumab, several patients at our institution have experienced marked improvements with IL-6 blockade. Several clinical trials of agents that block IL-6 are ongoing or near completion. 11

References:

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Elsevier

International Journal of Infectious Diseases

Case report case report study of the first five covid-19 patients treated with remdesivir in france.

Remdesivir has been found to be potent in vitro inhibitor of RNA viruses including SARS-CoV-2, but its in vivo potency is still under investigation.

This study report the clinical and biological features of five patients hospitalized with COVID-19 and treated with remdesivir for compassionate use.

For two patients, viral loads in nasopharyngeal samples decreased, despite active replication in the lower respiratory tract area.

The treatment had to be interrupted in four of the five patients, because of ALT elevation and/or renal failure.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been identified as the virus responsible for the coronavirus disease 2019 (COVID-19) outbreak worldwide. Data on treatment are scare and parallels have been made between SARS-CoV-2 and other coronaviruses. Remdesivir is a broad-spectrum antiviral with efficient in vitro activity against SARS-CoV-2. Evidence of clinical improvement in patients with severe COVID-19 treated with remdesivir is controversial. The aim of this study was to describe the clinical outcomes and virological monitoring of the first five COVID-19 patients admitted to the intensive care unit of Bichat-Claude Bernard University Hospital, Paris, France, for severe pneumonia related to SARS-CoV-2 and treated with remdesivir. Quantitative reverse transcription PCR was used to monitor SARS-CoV-2 in blood plasma and the lower and upper respiratory tract. Among the five patients treated, two needed mechanical ventilation and one needed high-flow cannula oxygen. A significant decrease in SARS-CoV-2 viral load in the upper respiratory tract was observed in most cases, but two patients died with active SARS-CoV-2 replication in the lower respiratory tract. Plasma samples were positive for SARS-CoV-2 in only one patient. Remdesivir was interrupted before the initialy planned duration in four patients, two because of alanine aminotransferase elevations (3 to 5 normal range) and two because of renal failure requiring renal replacement. This case series of five COVID-19 patients requiring intensive care unit treatment for respiratory distress and treated with remdesivir, highlights the complexity of remdesivir use in such critically ill patients.

Cited by (0)

Marie Dubert and Benoit Visseaux contributed equally to this work as first authors.

Jade Ghosn and Francois-Xavier Lescure contributed equally to this work as last authors.

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'COVID-22' Case Studies: What Can We Learn From Them?

Colas tcherakian, md.

November 15, 2022

We’re once again seeing patients in hospital with severe cases of COVID-19, despite being triple vaccinated and not being immunocompromised. Colas Tcherakian, MD, respiratory medicine specialist at the Foch Hospital, Paris, France, presents two recent COVID case studies and explains why this new wave is similar to the first. What lessons can be learned?

This transcript has been edited for clarity.

Good morning, I’m Colas Tcherakian, a respiratory medicine specialist at Foch Hospital, and I’m going to discuss two cases that reflect what we’re seeing quite often nowadays. I’ve called them "COVID-22 case studies" because it's 2022 and the virus has changed a lot since the COVID-19 we first heard about. Nowadays, this "COVID-22" reminds us of what we were faced with in 2020, during the first wave of the pandemic. But, in what way? Because this eighth wave has now plateaued and we’re seeing patients that we weren't seeing before. Once again, we’re seeing seriously ill patients with no apparent comorbidities, who are not immunocompromised and have been vaccinated. We need to look at these patients because I think they can teach us several things.

Patient One: Severe COVID in a Triple-Vaccinated Patient

Let's look at the first patient, a 59-year-old male. He had very little previous history, uncomplicated dyslipidemia, and, what's more, he was only receiving treatment for this with a lipid-lowering drug. He is a smoker. This is very important, because we know that smoking is still a risk factor for COVID complications. He has smoked 10 cigarettes a day for around 30 years. He started with mild symptoms, with cough, shortness of breath, and a fever. When his fever worsened, the patient used over-the-phone medical services to speak with a doctor who prescribed corticosteroids and Augmentin (amoxicillin/clavulanic acid). Despite starting this treatment, the patient's condition worsened over the following days. After seeing his family physician, who found the patient's oxygen saturation to be low, he was referred to the hospital's emergency department.

In this patient we see features that some of us know very well: a mixture of typical features of COVID with some signs of organizing pneumonia about to appear in a patient with hypoxemia. One important point to note is that his D-dimers were very high, and a small pulmonary embolism was detected. In short, a clinical picture that would have been completely classic in 2020, the only difference being that this patient has received three vaccine doses. The fact that he’d indeed received three vaccine doses is likely to be significant. We know he’s had them because his COVID serology results were very positive at more than 5000 BAU. This means he couldn't be more protected in terms of antibodies. We’ve talked about this in a previous Medscape video. Namely, that high antibody levels are not a given for protection and, what's more, I advised against testing antibody levels to determine whether to further vaccinate a patient. This patient is proof of this. There is no good antibody-protection correlation. You can have no antibodies and a good cellular response and not be infected and, like in this patient’s case, have antibody levels through the roof and still develop a severe form of COVID.

However, we weren't seeing these latter types of patients anymore, so what’s changed? Is it because the patient had his last dose of the vaccine too long ago? We know that, more than the level of antibodies, it's probably the time from the last dose that is the predictive factor in getting COVID. We had a rule that said, "if you have no comorbidities, are not immunocompromised, and have had three doses, you won’t end up in hospital." And this was true until the latest wave, the seventh, when we stopped seeing this type of patient.

So, is it because he had his last vaccine dose too long ago (November 2021)? Is this a new variant — BQ.1.1 — with some features like that of the Wuhan virus, with lung tropism and a secondary risk of embolism? This is something to consider. I think how the wave progresses will confirm whether we’re likely to see more patients like this.

Patient Two: COVID With Lung Lesions in a Patient on DOACs

Another case, that of a 69-year-old male patient who, this time, has a more extensive medical history. It includes a history of strokes, the aftereffects of which have been minimal atrial fibrillation. What is very interesting in this patient is that he is being treated with direct-acting oral anticoagulants (DOACs) and he is also an active smoker — six to seven cigarettes per day. We must remember smoking is a risk factor, contrary to what was initially reported.

Whilst having COVID, the patient also had a small pulmonary embolism with a second feature — lung lesions. We’ve already described this with the typical form of COVID, where you could just have COVID in the form of a pulmonary embolism with, sometimes, very significant clots and no parenchymal lesions. And so, we would say to ourselves: "be careful, any patients with a pulmonary embolism during the COVID epidemic must be tested for COVID." Why? Because if you’re positive for COVID, this means it’s a predisposing factor and the patient will only be treated for 3 months. Conversely, if COVID is not detected and the pulmonary embolism cannot be explained, you will start a more long-term treatment plan. So, it's always worth doing a COVID PCR on a patient with a pulmonary embolism during the COVID epidemic, even if they have no lesions, few symptoms, and no fever.

In this case, once again we had a triple-vaccinated patient with an embolism and signs of inflammation, whose vaccination status was confirmed by positive serology results (590 BAU), which is the level it should be at. So, we have found a slightly different type of patient, but with the same features. COVID can cause embolism, even in patients on DOACs. That's why [low molecular weight heparin] (LMWH) was initially proposed during the acute phase, because we’ve never had a relapse on a LMWH, unlike with DOACs.

So, we have a second type of patient, with an isolated pulmonary embolism, including those on anticoagulants, and these should be monitored.

The point of this discussion isn't necessarily to cause alarm, but to say that today we seem to be detecting COVID again as we saw before, and this is probably worth discussing, as well as facilitating vaccination for those patients whose last vaccine dose was over 6 months ago. It also perhaps appears that those with no comorbidities, whom we felt were quite safe, may now be at more risk than before. 

So, be alert and stop thinking that current COVID types, and probably BQ.1.1, are just a cold, as we believed at one time for patients who had just been vaccinated, as well as being under the impression that we would no longer see that type of COVID in a hospital setting.

Thank you. I’ll be back to discuss vaccination.

This content was originally published on Medscape French edition.

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