ABSTRACT
Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are point-of-care viscoelastic tests of whole blood that provide real-time analyses of coagulation. TEG and ROTEM are often used to guide blood product administration in the trauma and surgical settings. These tests are increasingly being explored for their use in other disease states encountered in critically ill patients and in the management of antithrombotic medications. As the medication experts, pharmacists should be familiar with how to interpret and apply viscoelastic tests to disease state and medication management. The purpose of this narrative review is to provide a primer for pharmacists on viscoelastic tests and their interpretation and to explore non-trauma indications for viscoelastic testing in critical care. Literature evaluating the use of TEG and ROTEM for patients with acute and chronic liver disease, ischemic and hemorrhagic stroke, myocardial infarction, cardiac arrest, coronavirus disease 2019, and extracorporeal membrane oxygenation are described. Current applications of viscoelastic tests by pharmacists and potential future roles of critical care pharmacists in expanding the use of viscoelastic tests are summarized.Copyright © 2023 The Authors. JACCP: Journal of the American College of Clinical Pharmacy published by Wiley Periodicals LLC on behalf of Pharmacotherapy Publications, Inc.
ABSTRACT
Aim. To determine the prevalence and show the features of the development of newly diagnosed heart failure (HF) in patients with dyspnea after a coronavirus disease 2019 (COVID-19). Material and methods. This clinical prospective observational study was conducted during 2020-2022. The study consecutively included 368 outpatients with shortness of breath, who applied to the clinic. Depending on the presence of prior COVID-19, the patients were divided into 2 groups: the first group consisted of 205 patients with shortness of breath after COVID-19, the second group - 163 patients without prior COVID-19. All patients underwent a clinical examination within 3 days after presentation with an assessment of outpatient records and other medical documents for the differential diagnosis of dyspnea. The severity of dyspnea was determined using the Modified Medical Research Council Dyspnoea Scale (mMRC). The diagnosis of HF was verified in accordance with the 2020 Russian Society of Cardiology guidelines and in some cases reclassified in accordance with the 2021European Society of Cardiology guidelines. For further analysis, 2 subgroups of patients with HF were identified depending on the presence and absence of prior COVID-19. The subgroup analysis excluded patients with acute heart failure, acute illness, and conditions requiring hospitalization and/or intensive care. Results. Among 368 patients who presented to the clinic with dyspnea during 2020-2022, 205 patients (55,7%) had COVID-19. The average period of treatment after COVID-19 was 3,5 [1,5;22,4] months. Patients after COVID-19 applied earlier after the onset of dyspnea, which is associated with higher mMRC score. The prevalence of HF among patients with shortness of breath after COVID-19 was significantly higher than in patients without this pathology in history, and amounted to 19,0% vs 9,8% (p=0,021). Prior COVID-19 increased the relative risk (RR) of HF in patients with shortness of breath by 1,7 times. RR for HF in systolic blood pressure >140 mm Hg increased by 1,9 times, while in diastolic blood pressure >90 mm Hg - by 1,9 times, with the development of a hypertensive crisis - by 28%, with a heart rate >80 bpm at rest - by 1,4 times, with the development of type 2 diabetes - by 31%, in the presence of pulmonary fibrosis - by 2,3 times. Patients with shortness of breath after COVID-19 had more severe HF, both according to clinical tests and according to the blood concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP), mainly with the preserved ejection fraction (EF) with a higher prevalence of left atrial (LA) enlargement in combination with a decrease in right ventricular (RV) systolic function and its dilatation. In patients after COVID-19 in the presence of chronic kidney disease, the RR for HF increased by 4,5 times;in the presence of C-reactive protein >4 mg/l - by 1,6 times. Conclusion. Every fifth patient with shortness of breath 3,5 months after COVID-19 had more severe HF, both according to clinical tests and according to blood NT-proBNP concentration, mainly with preserved EF with a higher prevalence of LA increase in combination with a decrease in RV systolic function and its dilatation. The risk of HF is interrelated with the female sex and multiple comorbidities.Copyright © 2023, Silicea-Poligraf. All rights reserved.
ABSTRACT
Background: SAMD9L is a tumor suppressor involved in regulating the proliferation and maturation of cells, particularly those derived from the bone marrow, and appears to play an important role in cerebellar function. It can be activated in hematopoietic stem cells by type I and type II interferons. It has been hypothesized to act as a critical antiviral gatekeeper regulating interferon dependent demand driven hematopoiesis. Gain of function mutations can present with an immunodeficiency due to transient severe cytopenias during viral infection. Case presentation: We report a 3-year-old boy born full term with a history of severe thrombocytopenia requiring transfusions, developmental delay, ataxia, seizure disorder, and recurrent severe respiratory viral infections. His infectious history was significant for respiratory syncytial virus with shock requiring extracorporeal membrane oxygenation complicated by cerebral infarction and a group A streptococcus empyema, osteomyelitis requiring a left below the knee amputation, and infections with rhinovirus, COVID-19, and parainfluenza requiring hospitalizations for respiratory support. Initial immunologic evaluation was done during his hospitalization for parainfluenza. His full T cell subsets was significant for lymphopenia across all cell lines with CD3 934/microL, CD4 653/microL, CD8 227/microL, CD19 76/microL, and CD1656 61/microL. His mitogen stimulation assay to phytohemagglutinin and pokeweed was normal. Immunoglobulin panel showed a mildly decreased IgM of 25 mg/dL, but normal IgA and IgG. Vaccine titers demonstrated protective titers to 12/22 pneumococcus serotypes, varicella, diphtheria, mumps, rubella, and rubeola. Repeat full T cell subsets 6 weeks later revealed marked improvement in lymphocyte counts with CD3 3083/microL, CD4 2101/microL, CD8 839/microL, CD19 225/microL, and CD1656/microL. A primary immunodeficiency genetic panel was ordered and positive for a heterozygous SAMD9L c.1549T>C (p.Trp517Arg) mutation classified as a variant of unknown significance. Discussion(s): This patient's history of severe viral infections, ataxia, thrombocytopenia, and severe transient lymphopenia during infection is suggestive of a SAM9DL gain of function mutation. Protein modeling done by the laboratory suggests this missense mutation would affect protein structure. The mutation found has been observed in individuals with thrombocytopenia. This case highlights the importance of immunophenotyping both during acute illness and once recovered.Copyright © 2023 Elsevier Inc.
ABSTRACT
Objectives: Healthcare systems require comprehensive data for long-term resource allocation planning to support people living with post-COVID-19 condition (PCC). Limited information is available on long-term PCC-associated healthcare utilization patterns. In this study, we assess healthcare utilization rates six and 12-18 months following acute COVID-19 illness among COVID-19 survivors in British Columbia (BC), Canada by PCC status. Method(s): We used difference-in-difference analysis to assess healthcare utilization by all adult COVID-19 survivors in BC diagnosed with COVID-19 on/before November 18, 2021 during three time periods: (i) 26 weeks after the first 4 weeks of COVID-19 illness, and that exact period (ii) one or two years prior (baseline), and (iii) one year afterwards. PCC/non-PCC patients were matched 1:2 on age, sex, region, comorbidities, vaccination status, and COVID-19 index date +/-14 days. The total number of daily healthcare encounters (medical visit, emergency department visit, hospitalization) per person was calculated. Rate ratios (RR) for PCC-associated healthcare utilization were estimated using weighted Poisson regression. Result(s): The matched cohort (n= 7,092) included 2,364 PCC patients (54.9% female;mean age 39.8 [SD, 13.4] years). Healthcare utilization rates were comparable between the PCC and non-PCC groups at baseline (average: 39.3 vs. 32.7 visits per 1000 patients, respectively), but rose two-fold for the PCC group during the 26-week period post-acute illness (76.1 vs. 33.5). One year later, PCC-associated healthcare utilization rates declined but remained elevated relative to baseline rates (54.6 vs. 34.4). In multivariable Poisson regression models, PCC was associated with a 103% increase in healthcare utilization over 26 weeks post-acute illness (aRR: 2.03, 95% CI 1.71-2.41) and a 24% increase the next year (aRR: 1.24, 95% CI 1.03-1.48). Conclusion(s): The increased healthcare utilization rates noted among PCC patients one year following acute COVID-19 illness highlights the need for adequate planning to provide optimal support for people living with PCC.Copyright © 2023
ABSTRACT
Objective: Hypercoagulation and high incidence of thrombosis during COVID-19 is well established. However, there is a lack of data, how it changes over time. The main purpose of our study was to access different parts of hemostasis in few months after acute disease. Material and methods. Patients discharged from our hospital were invited for follow up examination in 2,3-3,8 (group 1 - 55 pts) or 4,6-5,7 months (group 2 - 45 pts) after admission. Control group (37 healthy adults) had been collected before pandemic started. Standard coagulation tests, aggregometry, thrombodynamics and fibrinolysis results were compared between groups. Result(s): D-dimer was significantly higher, and was APPT was significantly lower in group 2 compared to group 1, while fibrinogen, prothrombin levels didn't differ. Platelet aggregation induced by ASA, ADP, TRAP, spontaneous aggregation didn't differ significantly between groups. Thrombodynamics revealed hypocoagulation in both group 1 and group 2 compared to control: V, mum/min 27,3 (Interquartile range (IQR) 26,3;29,4) and 28,3 (IQR 26,5;30,1) vs. 32,6 (IQR 30,4;35,9) respectively;all p < 0,001. Clot size and density in both group 1 and group 2 were significantly lower than in control group. Fibrinolysis appeared to be enhanced in x2 compared to control and group 1. Lysis progression, %/min was higher: 3,5 (2,5;4,8) vs. 2,4 (1,6;3,5) and 2,6 (2,2;3,4) respectively, all p < 0,05. Lysis onset time in both group 1 and group 2 was significantly shorter compared to control. Conclusion(s): We revealed normalization of parameters of clot formation process in 2-6 months after COVID-19, while fibrinolysis remained still enhanced. Further study is required to investigate the clinical significance of these changes.Copyright © Creative Cardiology 2021.
ABSTRACT
Objective: Studies have reported significant cognitive impairment following Covid-19, although the majority of reports rely on patients' self-report or short screening instruments to quantify cognitive function. Additionally, little is known about the development of cognitive impairment post Covid-19 and how these trajectories are related to psychiatric and medical variables. Method(s): Patients presenting a spectrum of neurological symptoms following Covid-19 infection were recruited from a national multicenter study. At 6 (N = 77) and 12 (N = 58) months post-covid infection, they completed a comprehensive neuropsychological assessment. At 6 months self-reported symptoms of cognitive dysfunction and fatigue were extracted from questionnaires and depression diagnoses from the MINI neuropsychiatric interview. A control group (N = 58), antibody verified Covid-19 negative, completed neuropsychological assessment. Result(s): At 6 months, verbal and visual memory, attention/working memory, and executive function were significantly reduced in patients compared to healthy controls. These impairments were not associated to acute illness severity indexes, and only moderately correlated to subjective cognitive complaints, level of fatigue, and diagnosis of depression at 6 months. There was a significant improvement in cognitive function across affected domains from 6 to 12 months post infection. This improvement was not associated with depression or self-report at 6 months, nor was the improvement related to acute illness severity. Conclusion(s): Covid-19 patients presenting with neurological symptoms showed significant cognitive impairment at 6 months. However, at 12 months their cognitive functions were normalized and no longer different from healthy controls. These results indicate a good prognosis regarding cognitive function in most patients following Covid-19 infection.Copyright © 2023
ABSTRACT
Acute respiratory viral infections (ARVI) play an important role in morbidity formation among children. At the same time, studies about the ARVI etiological structure are not enough. The article presents the results of structure analyses of ARVI in children with severe and moderate degrees of disease hospitalized in the children's clinical hospital of Novosibirsk for the period 2015-2018. This research aimed to analyze the morbidity of acute respiratory viral infections with the estimation of a causal virus in children admitted to the hospital for the period 2015-2018. Material and methods. In this study, 1137 children aged between 0 and 15 years were examined. In order to determine the etiological factor in children with damage of the upper or lower respiratory tract, by using the method of RT-PCR (AmpliSensARVI-screen-FL test systems (InterLabService, Russia), mucus from the nose and throat was examined for the presence of genetic material of viruses that cause ARVI (influenza A and B viruses, parainfluenza viruses of types 1-4, respiratory syncytial virus, metapneumovirus, four types of human coronavirus, rhinovirus, adenovirus, and bocavirus). Results. The research found that the most frequently detected pathogens are respiratory syncytial virus (23.52%), influenza A and B viruses (19.73%) and rhinovirus (19.21%). Observe the dynamics some fluctuations in the detection of mentioned viral agents and increasing of mixed infections were detected. In addition, the importance of respiratory and gastrointestinal tract combined lesions, particularly for infants and preschool - age children has been noted. Conclusion. The distribution of respiratory viruses in children with severe ARVI who required hospitalization was assessed. It was shown the significance of the respiratory syncytial infection virus, influenza virus and rhinovirus in the etiological structure of hospitalized children of different ages that damage not only the respiratory tract, but also to the gastrointestinal tract. This is an important factor in optimizing the diagnosis, treatment and prevention of viral infections in children.Copyright © Infectious Diseases: News, Opinions, Training 2021.
ABSTRACT
Purpose of Study: The regional NICU is an essential healthcare resource for families of newborns with serious life-threatening illnesses. Mechanical ventilation, cardiovascular therapies, therapeutic hypothermia, and neonatal surgeries are common life-sustaining interventions. Our NICU serves an underprivileged population in a resource poor environment and several ethical questions frequently emerge when facing extremes of innovative therapies. The pandemic and rapidly changing institutional protocols accentuated challenges faced by frontline NICU teams caring for newborns at risk for devastating illnesses and death. Concurrently, evolving paradigms in neonatal ethics required urgent and high quality palliative care in a background of racial and socioeconomic inequities, restrictive visitation policies, and limited healthcare resources. The purpose of this study was to ensure that neonates and their families receive ethically sound care, timely referrals for innovative therapies, and specialized palliative care in the strained and uncertain environment of the COVID-19 pandemic. Methods Used: The key steps consisted of structured and impromptu discussion forums for specialized palliative care and medical ethics, perinatal case conferences and pediatrics grand rounds on virtual platforms, educational webinars for interdisciplinary teams, and improved electronic communication. Online collaboration and innovative combinations of in-person and virtual meetings were utilized for urgently Incorporating clinical updates. Summary of Results: 1. A neonate with severe HIE and postnatally diagnosed congenital diaphragmatic hernia required emergent ECMO center referral. NICU providers utilized a structured bioethics and palliative care framework for providing family support and discussing the prognostication challenges of acute illnesses. 2. Many important bioethical questions emerged while caring for infants with life-threatening chromosomal abnormalities. Ethical tension was addressed by teaching tools, quality of life and pediatrics ethics conversations, mitigation of moral distress, contemporary clinical and surgical experience, community engagement, and family perspectives. 3. Ethical conflicts are central in the decision to resuscitate neonates born between 22 and 23 weeks of gestation. To provide urgent prenatal consultations and attend high risk deliveries, we collaborated across geographically distant healthcare systems, unified management strategies and analyzed outcomes data. 4. NEC in several extremely preterm babies had devastating outcomes and the team respected each family's voice with compassionate, shared decision-making for both curative care surgeries and palliative care. Conclusion(s): The new workflows, telephone and video conferences, and redirection to telehealth based family meetings did not change important outcomes during the pandemic. Advocacy and education for integrating bioethics and palliative care were vital facets of neonatal critical care in a resource poor and ever-changing pandemic environment.
ABSTRACT
Purpose of Study The detrimental long-term effects of obesity are well-described in literature;however, there has been recently emerging evidence describing a possible mortality benefit in obese patients with acute injury. The scope of this review is to provide an overview of the ongoing debate surrounding this observation. We focused our discussion on evaluating the evidences suggesting an impact of obesity and overweight on multiple acute medical conditions. Methods Used We searched the PubMed database with the keywords 'obesity', 'paradox', 'trauma', 'mortality', 'BMI', 'cancer', 'sepsis', 'lung injury', 'stroke', 'COVID', and 'myocardial infarct' from inception to 2020 and selected 40 relevant papers discussing the relationship between mortality and BMI in the setting of these stressors, and the mechanisms behind them. Summary of Results Amongst the fields of blunt trauma, cardiovascular disease, cancer, and critical care admissions for sepsis and lung injury, there are a growing amount of evidences supporting the existence of a paradoxical mortality benefit with overweight and mild obesity compared to normal and lean BMI. These findings must be attenuated with study design and BMI limitations, as well as biases prevalent throughout these studies. Although several hypotheses have been proposed, the exact mechanisms behind this relationship are largely unknown. Conclusions This survey of the obesity paradox shows promise in regard to overweight and mild obesity helping with survival post-acute illness, possibly due to metabolic reserves, antiinflammatory, and anti-oncogenic conditions seen in obesity. We recommend addressing current major limitations by having future studies prospectively designed to evaluate alternative body weight metrics such as waist-to-hip ratio or waist circumference, with special attention to the timing of body weight measurements and its progression in the patient's life. In the future, elucidating the biological mechanisms of this relationship may allow us to adapt our recommendations to the patients and help direct optimal therapeutic approach in the management of certain acute pathologies.
ABSTRACT
Introduction/Aim: Reduced carbon monoxide diffusing capacity (DL CO) is common after recovery from severe COVID-19 and cohort studies have found it to be more abnormal than either VC or TLC. There is no specific evidence that this relates to membrane disfunction or vascular injury. Concurrent measurement of nitric oxide diffusing capacity (DL NO) and DL CO can be used to partition gas diffusion into its two components - membrane conductance (D m CO) and capillary blood volume (V C). In this study, we sought to evaluate D m CO and V C in the early and later recovery periods after severe COVID-19. Method(s): Patients attended for post-COVID outpatient clinical review and complex lung function testing including DL NO /DL CO (Hyp'Air;Medisoft, Leeds). Further appointments and repeat testing occurred when indicated. Lung function comparisons were made using t-tests. Result(s): 46 (8 female) subjects (mean+/-SD age 58+/-13, BMI 34+/-8), who had severe COVID pneumonitis, WHO ordinal severity classification of 6+/-1 and prolonged (19+/-22 days) length of hospital stay, were assessed 51+/-29 days post discharge. Mean TLC [z-score -1.64+/-1.31] and D L CO [z-score -1.60+/-1.48] were both reduced. V C and D m CO were reduced to a similar extent (Z-score -1.36+/-1.19 and -1.14+/-1.06, p=0.4). 14 (1 female) patients returned for testing 70+/-35 days later. In this subgroup, D L CO improved but remained below LLN (Z-score -2.98+/-0.73 [Visit 1] Vs -2.17+/-0.69 [Visit 2], p=0.01). D m CO improved (Z-score -1.99+/-0.91 Vs -1.25+/-1.17, p=0.01) but V C was unchanged (Z-score -2.33+/-0.53 Vs -2.03+/-0.76, p=0.17). Conclusion(s): Gas exchange is persistently abnormal after severe COVID. Membrane conductance is abnormal in the earlier recovery phase but improves to a significant extent. In contrast, reduced capillary blood volume persists. Repeat testing at longer intervals after recovery from acute illness is still required but these data raise the possibility that persisting effects of acute vascular injury will contribute to physiological impairment long after severe COVID pneumonitis.
ABSTRACT
The aim of this research is to describe the use of telemedicine applied to patients characterised by a particular state of illness, which often drives them toward a frail and chronic status, in a systematic manner. This work employed the Tranfield approach to carry out a systematic literature review (SLR), in order to provide an efficient and high-quality method for identifying and evaluating extensive studies. The methodology was pursued step by step, analysing keywords, topics, journal quality to arrive at a set of relevant open access papers that was analysed in detail. The same papers were compared to each other and then, they were categorised according to significant metrics, also evaluating technologies and methods employed. Through our systematic review we found that most of the patients involved in telemedicine programs agreed with this service model and the clinical results appeared encouraging. Findings suggested that telemedicine services were appreciated by patients, they increased the access to care and could be a better way to face emergencies and pandemics, lowering overall costs and promoting social inclusion.Copyright © 2022 Inderscience Enterprises Ltd.
ABSTRACT
Introduction/Aim: Significant long-term effects on both symptomatology and respiratory function have been recognised in adult populations after COVID-19 infection, termed 'Long COVID'. These have caused loss of productivity and increased need for healthcare services. This study aimed to measure symptoms and lung function in children and adolescents after acute COVID-19 infection Methods: Between June 1 and 31 October 2021 there were 144 children admitted to hospital across the Sydney Children's Hospital Network, Australia. Of these, 63 children were referred to the respiratory clinic with symptoms of ongoing cough, shortness of breath and fatigue, 3-6 months post COVID infection. 20 of these children performed reliable lung function. For these children, body plethysmography and double diffusion testing were performed within 3-6 months of their infection. The Liverpool respiratory questionnaire and PROMIS paediatric sleep questionnaires were also administered. Result(s): Of the 20 patients tested, 7 had COVID pneumonitis requiring hospitalisation during the acute illness. 6 of the 20 patients had significant persistent symptoms as measured by the Liverpool respiratory questionnaire, while none of the children had any significant sleep symptoms. All children had preserved spirometry within normal limits. Of note, 2 children with persistent respiratory symptoms had DLNO/DLCO ratio >1.15, suggesting pulmonary vascular disease. The same two children who had elevated DLNO / DLCO had high ventilator equivalents on CPET testing suggesting increased physiological dead space ventilation. Despite this, their peak aerobic capacity was within normal limits. There were no significant differences between the alpha and delta cohorts or between children treated at home vs those requiring hospitalisation during their infection. Conclusion(s): COVID-19 may cause long-lasting effects in children. In this cohort, all children maintained spirometry results within normal limits despite significant symptoms impacting daily activities. Double diffusion testing may shed some light on lung changes leading to persistent symptomatology after COVID infection.
ABSTRACT
Introduction: The association between worse COVID-19 outcomes and diabetes has been well-established in the literature. However, with more cases of new-onset diabetes and pancreatitis being reported with or after COVID-19 infection, it poses the question if there is a causal relationship between them. Case Description: 31 y/o female with COVID-19 infection 4-6 weeks ago with moderate symptoms (not requiring hospital admission or monoclonal ab), presented to ED with bandlike epigastric pain radiating to back, which is worsened with food, associated with nausea, vomiting, polyuria, and fatigue. Workup showed lipase 232, AST 180, ALT 256. Blood glucose was 281 and HbA1c was 12. CT A/P showed post cholecystectomy status, normal pancreas with mesenteric adenitis. MRCP showed hepatic steatosis with trace fluid around the pancreas s/o inflammation, and no evidence of choledocholithiasis or biliary dilatation. She denied alcohol use and autoimmune workup for pancreatitis was unremarkable. Islet cell antibodies were negative. The patient improved with fluid resuscitation and was discharged home on insulin with plans to transition to oral agents outpatient. Discussion(s): Long COVID is defined as a range of conditions or symptoms in patients recovering from COVID-19, lasting beyond 4 weeks after infection. A retrospective cohort study showed increased new-onset diabetes incidence in patients after COVID-19. This was redemonstrated in a systematic review and meta-analysis that showed a 14.4% increased proportion of new diagnoses of diabetes in patients hospitalized with COVID-19. Possible pathophysiology that have been attributed to this include undiagnosed pre-existing diabetes, hyperglycemia secondary to acute illness and stress from increased inflammatory markers during the cytokine storm, the effect of viral infections on the pancreas, and concurrent steroid use in patients with severe respiratory disease. The binding of SARS-CoV-2 to ACE2 receptors is thought to the other mechanism by which COVID can cause pancreatitis and hyperglycemia. Study showed increased lipase and amylase levels in patients with COVID and the increase in serum levels was proportional to the severity of the disease. Patients who died due to COVID-19 were also found to have degeneration of the islet cells. While, several studies have showed new onset diabetes and pancreatitis during an active COVID infections, we need larger cohort studies to comment on its true association or causation, especially in patients with long COVID symptoms. As more cases of new onset diabetes and pancreatitis with COVID-19 are being reported, there may be a need for more frequent blood sugar monitoring during the recovery phase of COVID-19.Copyright © 2023
ABSTRACT
Introduction/Aim: SARS-CoV-2 (COVID-19) has affected over 60 million people world-wide. In most cases symptoms are mild, however some people have ongoing symptoms lasting longer known as 'long COVID'. Exertional breathlessness is a common complaint in these patients. Dysfunctional breathing (DB) and vocal cord dysfunction (VCD) are two underappreciated causes of breathlessness. We hypothesized that in individuals who had experienced COVID-19, dysfunctional breathing could give rise to VCD. Method(s): Nine convenience-sampled participants with confirmed COVID-19 infection were included following resolution of the acute illness. Vocal cords movements were visualised via continuous laryngoscopy. Hyperventilation was employed as a surrogate for DB, using a standard protocol of 40 breathes per minute (bpm). Participants breathed through a flow sensor with concomitant laryngoscopy, and we monitored hyperventilation, gas exchange measurements and laryngeal movements. After 12-weeks patients returned for repeat hyperventilation testing. Result(s): The nine participants consisted of five females and four males, age range 24-66 years. Three of the nine participants developed classic inspiratory VCD during hyperventilation. Patients with VCD were female, younger (<45), reported significantly reduced exercise tolerance post infection and had been physically very active prior to COVID infection. In two participants VCD associated with hyperventilation had resolved on laryngoscopy at 12-weeks. In these two participants who had VCD, breathlessness and reduced exercise tolerance resolved at 12-weeks following laryngeal retraining. In one person evidence of VCD and reduced exercise tolerance persisted post 12-weeks review. Conclusion(s): This study provides the first evidence that COVID-19 may facilitate VCD via DB, causing unexplained breathlessness. Our findings suggest that this disease process may be implicated in 'long COVID' and provide a rationale for therapies such as breathing and laryngeal retraining.
ABSTRACT
In the relatively short period of time since December 2019, hundreds of millions of people globally have been infected with SARS-CoV-2, irrespective of their age, gender or ethnicity. Over that time, numerous mutations of various degrees of virulence and patho-genicity have occurred. The course of COVID-19 infection, an acute disease caused by the virus, is rather varied, ranging from asym-ptomatic or symptoms of common viral respiratory diseases to critical, with multiorgan failure and high mortality in high-risk patients. The overall mortality of the disease is 1-2 %. Unlike other viral respiratory diseases, this infection is often associated with frequent and rather diverse clinical manifestations developing after the acute phase of the infection, that is, more than 28 days after its onset. These complications are observed in both individuals with mild illness treated at home and inpatients with severe to critical illness. They develop both early after acute infection and some time after recovering from the disease. This rather heterogeneous group of pathologies may affect various organs and organ systems, with respiratory tract involvement being the most common and one of the most serious complications. Severe respiratory post-COVID-19 complications often include respiratory tract infections, in particular pneumonia.Copyright © 2022, Trios spol. s.r.o.. All rights reserved.
ABSTRACT
Introduction/Aim: We previously reported impaired pulmonary gas exchange in acute COVID-19 patients resulting from both increased intrapulmonary shunt (SH) and increased alveolar dead space (AD) 1 . The present study quantifies gas exchange in recovered patients. Method(s): Unvaccinated patients diagnosed with acute COVID-19 infection (March-December 2020) were studied 15 to 403 days post first SARS-CoV-2 positive PCR test. Demographic, anthropometric, acute disease severity and comorbidity data were collected. Breathing room air, steady-state exhaled gas concentrations were measured simultaneously with arterial blood gases. Alveolar CO 2 and O 2 (P A CO 2 and P A O 2 ;mid-exhaled volume) determined;AaPO2, aAPCO2, SH% and AD% calculated. 2 Results: We studied 59 patients (33 males, Age: 52[38-61] years, BMI: 28.8[25.3-33.6] kg/m 2 ;median[IQR]). Co-morbibities included asthma (n = 2), cardiovascular disease (n = 3), hypertension (n = 12), and diabetes (n = 9);14 subjects smoked;44 had experienced mild-moderate COVID-19 (NIH category 1-2), 15 severe-critical disease (NIH category 3-5). PaCO 2 was 39.4[35.6-41.1] mmHg, PaO 2 92.1[87.1-98.2] mmHg;P A CO 2 32.8[28.6-35.3] mmHg, P A O 2 112.9[109.4-117.0] mmHg, AaPO 2 18.8[12.6-26.8] mmHg, aAPCO 2 5.9[4.3-8.0] mmHg, SH 4.3 [2.1-5.9]% and AD 16.6 [12.6-24.4]%. 14% of patients had normal SH (<5%) and AD (<10%);1% abnormal SH and normal AD;36% both abnormal SH and AD;49% normal shunt and abnormal AD. Previous severe-critical disease was a strong independent predictor for increased SH (OR 14.8[2.28-96], [95% CI], p < 0.01), increasing age weakly predicted increased AD (OR 1.18[1.01, 1.37], p < 0.04). Time since infection, BMI and comorbidities were not significant predictors (all p > 0.11). Conclusion(s): Prior COVID-19 was associated with increased intrapulmonary shunt and/or increased alveolar dead space in 86% of this cohort up to ~13 months post infection, with those with more severe acute disease, and older patients, at greater risk. Increased intrapulmonary shunt suggests persistent alveolar damage, while increased alveolar dead space may indicate persistent pulmonary vascular occlusion.
ABSTRACT
Outcomes: 1. Utilizing CRISIS approach, participants can employ a unique strategy to holistically support patients with poor coping in an acute life-threatening situation. 2. Utilizing the CRISIS approach, participants will apply an ethical tool to mitigate the incongruence that sometimes happens between two ethical principles-autonomy versus beneficence. Autonomy is not always in harmony with beneficence. We present a patient with decisional capacity hospitalized with acute reversible neuromuscular paralysis who refused treatment despite expected recovery. Her decision created moral distress for the clinicians. An improvised palliative strategy resolved the above dilemma. Case presentation: 68-year-old female admitted with new-onset unsteady gait, diplopia, and speech impairment on waking up. She was healthy until 3 weeks before admission, when she developed upper extremity numbness progressing to both legs after a COVID-19 infection. She had bulbar and axial muscle weakness and right oculomotor nerve palsy with ptosis. Positive ice pack and pyridostigmine test indicated myasthenia gravis (MG). During hospitalization, she required mechanical ventilation secondary to acute respiratory failure from progressive paralysis. Serum-negative MG diagnosed, given the response to IVIG and pyridostigmine. The patient, amid acute crisis, refused therapies and wanted to transition to DNR-comfort care despite understanding the reversibility of her illness. Her family members supported comfort care option. Neurology was conflicted with the patient's choice because MG was treatable. Palliative care, ethics, and neuropsychology consulted to establish decision-making capacity, goals-of-care, and holistic support. Intervention(s): Palliative team utilized the CRISIS approach to address the impasse between the patient and the clinicians: 1. Continue care, collaborate with the teams 2. Respond empathetically 3. Integrate patient's autonomy 4. Support holistically 5. Improvise a care plan 6. Sustain quality of life We validated patient's autonomy. We recommended allowing time for the patient/family to process her illness. We continued holistic support and symptom management and created an improvised multidisciplinary plan to help her cope with the acute illness. The above approach enabled her to opt for therapies instead of comfort care only, and she gradually recovered. Respecting patients' autonomy and incorporating beneficence via our intervention led to positive outcomes. The CRISIS approach could help other clinicians in the situation when conflict arises between autonomy and beneficence.Copyright © 2023
ABSTRACT
The coronavirus disease of 2019 (COVID-19) caused by SARS-CoV-2 virus led to a worldwide pandemic. Emergency use of an investigational medication, Paxlovid, was approved for patient 12 and older who tested positive for COVID-19 and at high risk for severe infection. Inflammatory Bowel Disease (IBD) is a chronic condition causing inflammation in the gastrointestinal tract. Ulcerative Colitis (UC) is a type of IBD centralized in colon and commonly treated with Immunosuppressive drugs. We present an adolescent with UC treated with paxlovid due to being on tacrolimus who developed with suspected tacrolimus toxicity. CASE REPORT: A 13-year-old female with UC presented to the ED with vomiting and fatigue after paxlovid ttreatment for COVID. The patient's UC treatment included tacrolimus along with ustekinumab. She had been diagnosed with SARS-CoV-2 and prescribed Paxlovid bid x 5 days due to immunosuppressive status. Tacrolimus was held during treatment. Once paxlovid completed, tacrolimus was restarted. Two days later, patient presented to ER for vomiting, fatigue, headaches and myalgia. Labs revealed a tacrolimus level of >60 ng/ml. Electrolytes and Creatinine were normal. Toxicology felt this was due to interaction between paxlovid and tacrolimus. Patient advised to hold tacrolimus for 48 hours and repeat levels were 15.8 ng/mL. Symptoms resolved and level repeated three days later and was 2.9 ng/mL. DISCUSSION: Tacrolimus is an immunosuppressant, commonly used for management of organ transplants but also been found effective in treatment of IBD. Tacrolimus requires close monitoring as toxicity may lead to acute or chronic kidney disease. The normal concentration is between 5-15 ng/mL. Due to rapid escalation of the COVID-19 pandemic, Paxlovid was approved for emergency use for treatment of high-risk patients. It is administered as a 5-day oral course consisting of nirmatrelvir and ritonavir. Our patient was prescribed Paxlovid due to risk secondary to immunosuppression. She was appropriately instructed to stop tacrolimus. Ritonavir is a cytochrome P450 3A inhibitor and can increase plasma concentration of tacrolimus. She restarted tacrolimus treatment 12 hours after her last dose of Paxlovid and presented with symptoms and a level consistent with toxicity. This level was concluded to be due to drug interaction between tacrolimus and Paxlovid. After further withholding of tacrolimus, symptoms improved, and levels normalized. Previous reports in transplant population stress importance of decreasing the dose of tacrolimus or withholding during the course of paxlovid treatment. This case demonstrates the importance of not only ceasing tacrolimus when administering paxlovid, but continuing discontinuation for longer period post completion of therapy to minimize interactions.Copyright © 2023
ABSTRACT
Background. SARS-CoV-2 infection can be accompanied by neuromuscular disorders. Rhabdomyolysis and Guillain-Barre syndrome have been described repeatedly. There are case reports of inflammatory myopathies manifesting during COVID-19, presenting as dermatomyositis, polymyositis or immune-mediated necrotizing myopathy, with dermatomyositis-like presentations most commonly reported. Larger cases series are from postmortem examinations of COVID-19 patients, where variable inflammatory pathology of the skeletal muscle has been found frequently but without local detection of the actual virus. Thus, autoimmune mechanisms or the systemic interferon response are discussed as causes. We report a case of focal inflammatory myopathy with perimysial pathology of the temporalis muscle occurring with acute, but mild COVID-19. Methods. Case report of clinical observations, cranial MRI, histopathological, and laboratory findings. 3T cranial MRI was performed with gadolinium contrast. Open temporalis muscle biopsy was performed. The sample underwent standard cryohistological studies as well as immunohistochemistry with antibodies against MHC-I and II, CD3, CD4, CD19, CD68, anti-MAC, p62 and MxA. Testing for auto-antibodies was based on immunoblots or ELISA. RT-PCR for SARS-CoV-2 was run with RNA extracted from cryopreserved muscle. Results. A Caucasian woman in her 60s with no history of autoimmune or muscle complaints developed swelling and pain of the right jaw musculature five days after testing positive for SARS-CoV-2 due to respiratory tract symptoms. In addition, she experienced trismus, but no further neuromuscular complaints. The course of respiratory tract symptoms stayed mild. She had been vaccinated previously with single shot SARS-CoV-2 vector vaccine. Due to persistent swelling and complaints, giant cells arteritis was excluded by unresponsiveness to five days oral steroids and sonography of the temporal artery. Cranial MRI was performed nearly four weeks after the SARS-CoV-2 infection and showed marked swelling and oedema of the temporalis muscle. Its biopsy showed numerous CD68 and acid phosphatase positive cells infiltrating from perimysial perivascular foci towards the endomysium with perimysial damage but little damage of adjacent, perifascicular muscle fibres. Muscle fibres did not react with anti-MHC-II, anti-MAC or -MxA. Capillaries did not react with anti-MAC or -MxA. SARS-CoV-2 RNA was not detected in muscle tissue. Serum creatine kinase was not elevated in the subacute phase. Slightly elevated ANA titre led to detection of autoantibodies against proliferating cell nuclear antigen (PCNA). No pathological results for other autoantibodies, including myositis-specific antibodies and anti-ds-DNA, were found in blood. Neither were antibodies against hepatitis C and B viruses. Retesting 15 weeks after infection, anti-PCNA immunoblot was still positive, but ELISA did not indicate a pathologic titre. The swelling, myalgia and trismus regressed spontaneously a month after onset, yet the latter still persists at the time of reporting. Conclusion. Our case diverges from the majority of COVID-19 associated my-ositis reports in the unusual location of the focal myositis and the histopathological pattern of predominantly perimysial damage and histiocytic infiltration. It concurs with the literature as no SARS-CoV2 RNA could be detected in the muscle. Anti-PCNA is associated very rarely with myositis. Other associated disorder (systemic lupus erythematosus, chronic viral hepatitis B or C) were not found. Increased levels of autoantibodies are reported in COVID-19 and mostly attributed to loss of self-tolerance during the acute disease phase. Interestingly, the structural protein M of SARS-CoV-2 appears to interact notably with PCNA in infected cells. Still, the causal connection between the myositis and COVID-19 in this case is based on the close temporal association in the absence of alternative, competing explanations from the medical history and findings.