What the Eye Cannot See: A Case of Persistent Altered Mental Status in a Patient With Cholestatic Liver Disease?

Introduction: Altered mental status (AMS) is a common symptom in patients with liver disease with a wide list of differential diagnoses. Knowledge of etiologies of AMS unique to patients with hepatic dysfunction is vital in order to help recognize, diagnose, and treat the underlying cause in a timely manner. Case Description/Methods: A 46-year-old man with a history of recent COVID infection was transferred to our hospital for further evaluation of acute liver injury and AMS. On arrival, his labs were notable for AST of 408 U/L, ALT of 620 U/L, ALP of 5942 U/L, TB of 11.0 mg/dL, and an INR of 1.1. His work-up included an MRCP that showed segmental biliary ductal dilation with associated restricted diffusion and peribiliary enhancement concerning for sclerosing cholangitis. ERCP revealed a 3cm biliary cast that was removed and noted diffuse rarefaction of ducts throughout the entire biliary tree. A liver biopsy revealed centrizonal cholestasis with portal-based bile ductular reaction and mild bile duct injury. Despite adequate treatment of suspected infection and hepatic encephalopathy, his AMS persisted. His basic metabolic panel (BMP) was notable for Na of 143 mEq/L. A send-out lipid panel that was obtained to work-up his dyslipidemia revealed a total cholesterol of 1018 mg/dL, triglycerides of 420mg/dL, and the presence of lipoprotein X. A venous blood gas (VBG) was obtained showing a Na of 157 mEq/L and serum osmolality was 322 mmol/kg, confirming true hypernatremia. He was slowly treated with hypotonic solutions with significant improvement in his mentation. On follow-up one year later, he has persistent cholestasis and is currently being considered for liver transplant. Discussion(s): The final diagnosis was COVID-related ischemic cholangitis and disappearing bile ducts with persistent cholangiopathy, presenting with severe cholestasis, accumulation of lipoprotein X, and pseudonormonatremia. When faced with severe cholestatic liver disease, clinicians should keep in mind the possibility of accumulation of lipoprotein X and its association with hyperviscosity and spurious electrolyte abnormalities. Clinicians should rely on obtaining blood gas analyses for accurate electrolyte measurement in such cholestatic patients as blood gas analyses utilize direct ion-sensitive electrodes (ISE) to measure electrolytes, whereas routine basic metabolic panels utilize indirect ISE that are liable to spurious results in the presence of hyperlipoproteinemia/lipoprotein X.

Association of blood viscosity and device-free days among hospitalized patients with COVID-19.

BACKGROUND: Increased estimated whole blood viscosity (eWBV) predicts higher mortality in patients hospitalized for coronavirus disease 2019 (COVID-19). This study assesses whether eWBV is an early predictor of non-fatal outcomes among patients hospitalized for acute COVID-19 infection. METHODS: This retrospective cohort study included 9278 hospitalized COVID-19 patients diagnosed within 48 h of admission between February 27, 2020 to November 20, 2021 within the Mount Sinai Health System in New York City. Patients with missing values for major covariates, discharge information, and those who failed to meet the criteria for the non-Newtonian blood model were excluded. 5621 participants were included in the main analysis. Additional analyses were performed separately for 4352 participants who had measurements of white blood cell count, C-reactive protein and D-dimer. Participants were divided into quartiles based on estimated high-shear blood viscosity (eHSBV) and estimated low-shear blood viscosity (eLSBV). Blood viscosity was calculated using the Walburn-Schneck model. The primary outcome was evaluated as an ordinal scale indicating the number of days free of respiratory organ support through day 21, and those who died in-hospital were assigned a value of -1. Multivariate cumulative logistic regression was conducted to evaluate the association between quartiles of eWBV and events. RESULTS: Among 5621 participants, 3459 (61.5%) were male with mean age of 63.2 (SD 17.1) years. The linear modeling yielded an adjusted odds ratio (aOR) of 0.68 (95% CI 0.59-0.79, p value < 0.001) per 1 centipoise increase in eHSBV. CONCLUSIONS: Among hospitalized patients with COVID-19, elevated eHSBV and eLSBV at presentation were associated with an increased need for respiratory organ support at 21 days. These findings are highly relevant, as they demonstrate the utility of eWBV in identifying hospitalized patients with acute COVID-19 infection at increased risk for non-fatal outcomes in early stages of the disease.

Blood hyperviscosity in acute and recent COVID-19 infection.

BACKGROUND: Elevated estimated blood viscosity (EBV), derived from hematocrit and globulins, is associated with thrombotic complications, organ failure, and higher mortality in COVID-19 patients. Although informative, EBV does not account for cellular interactions or fibrinogen. OBJECTIVE: Investigate whether patients with acute and recent COVID-19 have altered whole blood viscosity (WBV) when measured at both high and low shear rates using in vitro blood samples from patients. METHODS: Cross-sectional study of 58 patients: 15 in the intensive care unit with acute COVID-19, 32 convalescent (9 < 8weeks [W] from acute infection, 23 > 8 W), and 11 controls without COVID-19. WBV was measured at high (300 s-1) and low (5 s-1) shear rates (HSR, LSR) using a scanning capillary viscometer.RESULTSAcute and convalescent patients < 8 W had mean WBV at LSR (16.0 centipoise [cP] and 15.1 cP) and HSR (5.1 cP and 4.7 cP). Mean WBV of convalescent > 8 W and control patients were 12.3 cP and 13.0 cP at LSR, and 4.1 cP and 4.2 cP at HSR. Acute and < 8 W patients had significantly higher WBV at both HSR and LSR compared to patients > 8 W (all p≤0.01). No significant differences in WBV were observed between acute and < 8 W patients, or between patients > 8 W and controls. CONCLUSIONS: Hyperviscosity provides a possible explanation for thrombotic risk in acute and convalescent (< 8 W) patients. These findings have important implications for thromboprophylaxis.

Impact of neutrophil extracellular traps on fluid properties, blood flow and complement activation.

Introduction: The intravascular formation of neutrophil extracellular traps (NETs) is a trigger for coagulation and blood vessel occlusion. NETs are released from neutrophils as a response to strong inflammatory signals in the course of different diseases such as COVID-19, cancer or antiphospholipid syndrome. NETs are composed of large, chromosomal DNA fibers decorated with a variety of proteins such as histones. Previous research suggested a close mechanistic crosstalk between NETs and the coagulation system involving the coagulation factor XII (FXII), von Willebrand factor (VWF) and tissue factor. However, the direct impact of NET-related DNA fibers on blood flow and blood aggregation independent of the coagulation cascade has remained elusive. Methods: In the present study, we used different microfluidic setups in combination with fluorescence microscopy to investigate the influence of neutrophil-derived extracellular DNA fibers on blood rheology, intravascular occlusion and activation of the complement system. Results: We found that extended DNA fiber networks decelerate blood flow and promote intravascular occlusion of blood vessels independent of the plasmatic coagulation. Associated with the DNA dependent occlusion of the flow channel was the strong activation of the complement system characterized by the production of complement component 5a (C5a). Vice versa, we detected that the local activation of the complement system at the vascular wall was a trigger for NET release. Discussion: In conclusion, we found that DNA fibers as the principal component of NETs are sufficient to induce blood aggregation even in the absence of the coagulation system. Moreover, we discovered that complement activation at the endothelial surface promoted NET formation. Our data envisions DNA degradation and complement inhibition as potential therapeutic strategies in NET-induced coagulopathies.

Increased blood viscosity and red blood cell aggregation in patients with COVID-19

Background: Endothelial injury, hypercoagulability, and decreased blood flow are suspected to play a key role in thrombosis,multiorgan failure, and death of patients with COVID-19. The link between increased blood viscosity and COVID-19- related complications and severity is not formerly established and can only be suspected. Aim(s): The aim of this study was to (1) analyze blood viscosity, red blood cell (RBC) deformability, and aggregation in hospitalized patients with Coronavirus disease 19 (COVID-19);(2) test the associations between impaired blood rheology and blood coagulation;and (3) test the associations between impaired blood rheology and several indicators of clinical severity. Method(s): A total of 172 patients with COVID-19, hospitalized in COVID-unit of the Internal Medicine Department (Lyon, France) participated in this study between January and May 2021. Clinical parameters were collected for each patient. Routine hematological/ biochemical parameters, blood viscosity, RBC deformability and aggregation, and RBC senescence markers were measured on the first day of hospitalization. A control group of 38 healthy individuals was constituted to compare the blood rheological and RBC profile. Rotational thromboelastography was performed in 76 patients to study clot formation dynamics. Result(s): Our study demonstrated that patients with COVID-19 had increased blood viscosity despite lower hematocrit than healthy individuals, as well as increased RBC aggregation. In-vitro experiments demonstrated a strong contribution of plasma fibrinogen in this RBC hyper-aggregation. RBC aggregation correlated positively with clot firmness, negatively with clot formation time, and positively with the length of hospitalization. Patients with oxygen supplementation had higher RBC aggregation and blood viscosity than those without, and patients with pulmonary lesions had higher RBC aggregation and enhanced coagulation than those without. Conclusion(s): This study is the first to demonstrate blood hyper-viscosity and RBC hyper-aggregation in a large cohort of patients with COVID-19 and describe associations with enhanced coagulation and clinical outcomes.

COVID-19 and diabetes mellitus

COVID-19, a disease caused by the new Coronavirus SARSCoV-2, appeared in China in late 2019 and soon began to spread around the world. SARS-CoV-2 predominantly infects the airways, causing mild to severe symptoms, such as acute respiratory syndrome that can result in organ failure that eventually leads to death. The disease causes mild symptoms in most people, while it is dangerous for newborns, the elderly and immunocompromised people and people with comorbidities. Another epidemic is diabetes, which is growing dramatically worldwide: world estimates say that 463 million people between the ages of 20 and 79 live with diabetes, which over time develops chronic complications and risks of developing serious diseases and death. Diabetes mellitus is a chronic metabolic syndrome caused by an absolute and/or relative lack of insuhn, and is characterized by chronic hyperglycemia accompanied by disorders in the metaboHsm of carbohydrates, fats and proteins. Diabetes mellitus is accompanied by the development of various acute complications that occur suddenly and rapidly and require urgent intervention, and due to poor disease control and long-term hyperglycemia, chronic complications of diabetes occur as a result of damage to various tissues and organs, and are the main cause of morbidity and mortality in people with diabetes. People with diabetes are much more susceptible to SARS-CoV-2 virus infection and have a more severe clinical picture and poorer disease outcome after developing COVID-19. Some possible reasons are that SARS-CoV-2 infection can lead to increased levels of inflammatory mediators in the blood such as inflammatory cytokines, toxic metabolites and lipopolysaccharides and may modulate an already dysregulated immune response in diabetic patients. In addition, virus infection can lead to increased production of reactive oxygen species, fibrosis and acute lung damage, and acute respiratory distress syndrome. ROS production and viral activation of the renin-angiotensin-aldosterone system cause insulin resistance, hyperglycemia and vascular endothelial damage. There is also an increase in coagulation components, fibrinogen and D-dimer, which leads to increased blood viscosity and damage to the vascular endothelium and ultimately all this contributes to the development of cardiovascular problems, thromboemboHsm and disseminated intravascular coagulation (DIG). Drugs to lower blood glucose levels and those to dampen cytokine storm and lower lactate levels are useful for effective therapy in C O V I D patients with diabetes, and what would help prevent the development of the disease are improving metabolic health by changing diet and lifestyle. Copyright © 2022 Hrvatsko Farmaceutsko Drustvo. All rights reserved.

COVID-19 Demonstrates That Inflammation Is a Hyperviscous State.

Many of the complications of severe coronavirus disease-2019 (COVID-19) are caused by blood hyperviscosity driven by marked hyperfibrinogenemia. This results in a distinctive hyperviscosity syndrome which affects areas of high and low shear. A change in blood viscosity causes a threefold inverse change in blood flow, which increases the risk of thrombosis in both arteries and veins despite prophylactic anticoagulation. Increased blood viscosity decreases perfusion of all tissues, including the lungs, heart, and brain. Decreased perfusion of the lungs causes global ventilation-perfusion mismatch which results in silent hypoxemia and decreased efficacy of positive pressure ventilation in treating pulmonary failure in COVID-19. Increased blood viscosity causes a mismatch in oxygen supply and demand in the heart, resulting in myocarditis and ventricular diastolic dysfunction. Decreased perfusion of the brain causes demyelination because of a sublethal cell injury to oligodendrocytes. Hyperviscosity can cause stasis in capillaries, which can cause endothelial necrosis. This can lead to the rarefaction of capillary beds, which is noted in "long-COVID." The genome of the virus which causes COVID-19, severe acute respiratory syndrome coronavirus 2, contains an extraordinarily high number of the oligonucleotide virulence factor 5'-purine-uridine-uridine-purine-uridine-3', which binds to toll-like receptor 8, hyperactivating innate immunity. This can lead to a marked elevation in fibrinogen levels and an increased prevalence of neutrophil extracellular traps in pulmonary failure, as seen in COVID-19 patients.

MORPHOFUNCTIONAL CHARACTERISTICS OF BLOOD CELLS IN RECONVALESCENTS AFTER SUFFERING COVID-19.

Complexity and multifactorial nature of potential pathogenic consequences of SARS-CoV-2 infection in human body, discovery of new virus-induced mechanisms triggering a cascade of pathological responses in the cells of host organism leading to development of multiple organ failure elicited increasing interest in morpho-functional state of blood cells in reconvalescent persons after COVID-19 infection. The aim of the present work is to characterize morphofunctional pattern of blood cells at different periods of recovery, depending on the severity of COVID-19. We examined 55 convalescents after bearing COVID-19 infection: Group I included the convalescents 30 days after the disease (n = 39);Group II consisted of the persons 60 days after recovery (n = 16);Group III included clinically healthy volunteers with no history of clinical SARS- CoV-2 infection (n = 11). The cells were examined by means of Olympus CX41 microscope (Olympus, Japan), and VZ-C31S digital videocamera (VideoZavr, Russia) using the VideoZavr software (version 1.5). Assessment of neutrophil populations in the whole blood samples was performed with BD Accuri C6 Plus flow cytometer (USA) with automatic differentiation of cells between lymphocytes and monocytes, according to the degree of granularity. Cytokine production was determined using commercial kits for detection of IFNγ, TNFα, IL-4, IL-8, IL-10 (JSC Vector-Best, Russia), IL-17A (eBioscience, Austria) was assayed with automatic enzyme immunoassay analyzer “LAZURIT” (Dynex Technologies, USA). Among the convalescents who suffered the moderate-degree COVID-19 (45.5% and 50% of cases, respectively) on days +30 and +60 after clinical recovery, a significantly increased ratio of morphologically altered forms of erythrocytes (echinocytes, ovalocytes, dacryocytes, codocytes) was noted as compared with group III (p = 0.00001 and p = 0.001, respectively). Regardless of clinical severity of the disease;a mean of 40.6% convalescents from groups I and II had moderate disturbances in the neutrophil morphology (cytoplasmic vacuolization, chromatin decondensation at the pre- netosis stage, transformation of cells by the netosis type), and, in 27.4% of cases, the areas of neutrophil- platelet aggregation were seen. In blood supernates from recovered patients, we have revealed a significantly decreased content of IFNγ (p = 0.02), TNFα (p = 0.03), IL-10 (p = 0.04) and IL-17A (p = 0.02). The revealed morphological and functional changes in blood cells in the persons who underwent COVID-19 infection suggest long-term maintenance of toxic damage to erythrocytes, neutrophils and lymphocytes over the recovery period. The effects of the detected morphological and functional disorders of blood cells following COVID-19 recovery leading to increase in blood viscosity and microcirculation, formation of neutrophil-platelet aggregates, may cause higher risks of thrombotic complications at the long-range period as well as decreased levels of regulatory cytokines, thus confirming slow recovery of the lymphocyte populations (Th1, Th2, Th17) of the immune system. (English) [ FROM AUTHOR] Сложность и многофакторность реализации патогенного потенциала SARS-CoV-2 в орга- низме человека, раскрытие все новых механизмов, посредством которых вирус запускает каскад реак- ций в клетках макроорганизма, ведущих к формированию полиорганной недостаточности обусловили интерес к морфофункциональному состоянию клеток крови у реконвалесцентов после перенесен- ного COVID-19. Цель работы – охарактеризовать морфофункциональное состояние клеток крови в различный период реконвалесценции у пациентов в зависимости от степени тяжести перенесенного COVID-19. Обследовано 55 реконвалесцентов после перенесенного COVID-19: I группа – реконва- лесценты через 30 дней после болезни (n = 39);II группа – через 60 дней (n = 16);III группа – клини- чески здоровые добровольцы в анамнезе у которых отсутствовал факт заболевания, обусловленного SARS-CoV-2 (n = 11). Оценку состояния клеток проводили с помощью микроскопа Olympus CX41 (Olympus, Япония) и цифровой камеры VZ-C31S (VideoZavr, Россия) в программе VideoZavr (версия 1.5). Состояние популяции нейтрофильных гранулоцитов оценивали на проточном цитофлуориметре BD Accuri C6 Plus (США) в образцах цельной крови при автоматическом дифференцировании клеток от лимфоцитов и моноцитов по степени гранулярности. Продукцию цитокинов определяли с помо- щью коммерческих наборов для выявления IFNγ, TNFα, IL-4, IL-8, IL-10 (АО «Вектор-Бест», Рос- сия), IL-17A (eBioscience, Австрия) на автоматическом иммуноферментном анализаторе LAZURIT (Dynex Technologies, США). Среди реконвалесцентов, перенесших средне-тяжелую форму COVID-19 (45,5% и 50% случаев соответственно), на 30-е и 60-е сутки после клинического выздоровления от- мечали достоверное увеличение доли трансформированных форм эритроцитов (эхиноциты, овало- циты, дакриоциты, кодоциты) относительно III группы (p = 0,00001 и p = 0,001 соответственно). Независимо от тяжести течения болезни, в среднем у 40,6% реконвалесцентов I и II групп регистри- ровали умеренное нарушение морфологии нейтрофильных гранулоцитов (цитоплазматическая ваку- олизация,деконденсация хроматина на стадии преднетоза, трансформация клеток по типу нетоза), а в 27,4% случаев наблюдали участки нейтрофил-тромбоцитарной агрегации. Ð’ супернатантах крови реконвалесцентов выявлено достоверное снижение концентрации IFNγ (Ñ€ = 0,02), TNFα (Ñ€ = 0,03), IL-10 (Ñ€ = 0,04) и IL-17А (Ñ€ = 0,02). Выявленные морфофуРкциональные изменения клеток крови у лиц, перенесших COVID-19, свидетельствуют о длительности сохранения токсических повреждений эритроцитов, нейтрофилов и лимфоцитов в течение восстановительного периода. Влияние установ- ленных морфофункциональных нарушений клеток крови реконвалесцентов после перенесенного COVID-19, приводящих к повышению вязкости и микроциркуляции крови, формированию нейтрофил-тромбоцитарных агрегатов, вероятно, обусловливает риск развития тромботических осложне- ний в отдаленный период, снижение уровня регуляторных цитокинов, подтверждает медленное вос- становление лимфоцитарного звена (Th1, Th2, Th17) иммунной системы. (Russian) [ FROM AUTHOR] Copyright of Medical Immunology (1563-0625) is the property of National Electronic-Information Consortium and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

From the Oligonucleotide purUUpurU to Cytokine Storm, Elevated Blood Viscosity, and Complications of Coronavirus Disease 2019.

Background Coronavirus disease 2019 (COVID-19) can be associated with pathologic inflammation. The authors hypothesize that a high copy number of a purine-uridine-rich nucleotide motif is present in the genome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and hyperactivates innate immunity. Methods The number of purine-uridine-uridine-purine-uridine (purUUpurU) motifs was counted in the genomes of SARS-CoV-2 and other single-strand RNA viruses. The nucleotides of SARS-CoV-2 in random order were used as a control. Results PurUUpurU occurred 2.8 times more often in the actual SARS-CoV-2 genome than the randomized genome. The number of purUUpurU motifs correlates with the potential severity of acute illness caused by these viruses, except for influenza A. Conclusion The large number of purUUpurU in SARS-CoV-2 may hyperactivate innate immunity, potentially causing the markedly increased concentrations of cytokines, acute phase reactants, and blood viscosity that can be seen in COVID-19.

Association of Blood Viscosity With Mortality Among Patients Hospitalized With COVID-19.

BACKGROUND: Coronavirus disease-2019 (COVID-19) is characterized by a dysfunctional immune response and abnormal blood rheology that contribute to endothelial dysfunction and thrombotic complications. Whole blood viscosity (WBV) is a clinically validated measure of blood rheology and an established predictor of cardiovascular risk. We hypothesize that increased WBV is associated with mortality among patients hospitalized with COVID-19. OBJECTIVES: This study sought to determine the association between estimated BV (eBV) and mortality among hospitalized COVID-19 patients. METHODS: The study population included 5,621 hospitalized COVID-19 patients at the Mount Sinai Health System from February 27, 2020, to November 27, 2021. eBV was calculated using the Walburn-Schneck model. Multivariate Cox proportional hazards models were used to evaluate the association between eBV and mortality. Considered covariates included age, sex, race, cardiovascular and metabolic comorbidities, in-house pharmacotherapy, and baseline inflammatory biomarkers. RESULTS: Estimated high-shear BV (eHSBV) and estimated low-shear BV were associated with increased in-hospital mortality. One-centipoise increases in eHSBV and estimated low-shear BV were associated with a 36.0% and 7.0% increase in death, respectively (P < 0.001). Compared with participants in the lowest quartile of eHSBV, those in the highest quartile of eHSBV had higher mortality (adjusted HR: 1.53; 95% CI: 1.27-1.84). The association was consistent among multiple subgroups, notably among patients without any comorbidities (adjusted HR: 1.69; 95% CI: 1.28-2.22). CONCLUSIONS: Among hospitalized COVID-19 patients, increased eBV is significantly associated with higher mortality. This suggests that eBV can prognosticate patient outcomes in earlier stages of COVID-19, and that future therapeutics aimed at reducing WBV should be evaluated.

A raising dawn of pentoxifylline in management of inflammatory disorders in Covid-19.

The existing pandemic viral infection caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) leads to coronavirus disease 2019 (Covid-19). SARS-CoV-2 exploits angiotensin-converting enzyme 2 (ACE2) as an entry-point into affected cells and down-regulation of ACE2 by this virus triggers the release of pro-inflammatory cytokines and up-regulation of angiotensin II. These changes may lead to hypercytokinemia and the development of cytokine storm with the development of acute lung injury and acute respiratory distress syndrome. Different repurposed had been in use in the management of Covid-19, one of these agents is pentoxifylline (PTX) which has anti-inflammatory and antioxidant properties. Therefore, the objective of the present mini-review is to highlight the potential role of PTX in Covid-19 regarding its anti-inflammatory and antioxidant effects. PTX is a non-selective phosphodiesterase inhibitor that increases intracellular cyclic adenosine monophosphate which stimulates protein kinase A and inhibits leukotriene and tumor necrosis factor. PTX has antiviral, anti-inflammatory and immunomodulatory effects, thus it may attenuate SARS-CoV-2-induced hyperinflammation and related complications. As well, PTX can reduce hyper-viscosity and coagulopathy in Covid-19 through increasing red blood cell deformability and inhibition of platelet aggregations. In conclusion, PTX is a non-selective phosphodiesterase drug, that has anti-inflammatory and antioxidant effects thereby can reduce SARS-CoV-2 infection-hyperinflammation and oxidative stress. Besides, PTX improves red blood cells (RBCs) deformability and reduces blood viscosity so can mitigate Covid-19-induced hyper-viscosity and RBCs hyper-aggregation which is linked with the development of coagulopathy. Taken together, PTX seems to be an effective agent against Covid-19 severity.

Gaisbock in 2021

Case Report The purpose of the study is to explore the possible diagnosis of Gaisbock in a patient with long-standing erythrocytosis and hypertension. Methods Used Case Study Summary of Results A 40-year-old Caucasian man with obesity was admitted with recurrent leg swelling and increasing oxygen requirements two weeks after hospitalization with COVID-19 pneumonia. Upon review of the patient's history, he was found to have untreated hypertension over several medical encounters and an erythrocytosis spanning ten years. Recent medical history included a diagnosis of deep vein thrombosis (DVT) in the same leg two and a half months prior and was treated with Xarelto. The patient reported a history of low testosterone for 12 years. However, he had not used any testosterone supplementation for the last nine months. He reported daytime fatigue, frequent bouts of nighttime awakenings, and frequent snoring. The patient never had a sleep study or used a CPAP. The patient used half a can of chewing tobacco daily for thirteen years, and he smoked one pack per day for ten years but quit 12 years ago. He worked strenuous jobs in the construction industry most of his life. On this admission, the patient's lab work was notable for hemoglobin of 18.7 gm/dL (13.7-17.5) and a normal erythropoietin level of 5.7 MIU/mL (2.6-18.5) without thrombocytosis or leukocytosis and a positive factor V Leiden mutation. His blood pressure was 132/91 mmHg. On review of previous records, the patient was found to have consistently elevated hemoglobin The patient had a stocky, ruddy appearance without hepatosplenomegaly. Conclusion Erythrocytosis can be categorized as primary, secondary, or relative. Patients with relative erythrocytosis have a decreased plasma volume with a relative increase in hemoglobin. Additionally, elevated hemoglobin levels have been associated with hypertension. Gaisbock's syndrome, first described in 1905, is characterized by hypertension and erythrocytosis without splenomegaly, leukocytosis, or thrombocytosis. It is associated with mild obesity, elevated blood pressure, and increased blood viscosity, which may explain why these patients often develop cardiovascular complications. Patients with relative erythrocytosis are at a higher risk for thromboembolic complications. In this case, Gaisbock's syndrome was suspected because the patient had had a stocky, plethoric appearance with persistently elevated hemoglobin and blood pressure with a normal erythropoietin level. Gaisbock's syndrome establishes a relationship between benign erythrocytosis, hypertension, and an increased risk for cardiovascular events. (Table Presented).

Blood Viscosity in COVID-19 Patients With Sudden Deafness.

BACKGROUND: Changes in blood viscoelastic properties have been proposed previosuly as etiopathogenesis for severe complications in COVID-19 and some cases of Sudden Deafness (SD). This is an attempt to verify if SD cases in patients admitted for SARS-Cov-2 infection can be correlated. PATIENTS AND METHODS: A prospective follow-up was carried out with COVID-19 patients, monitoring their blood viscosity (BV) at high shear rate (300 s-1) and inquiring them periodically for eventual hearing loss. This measurement was extended to cases bearing of SD in 2019 and 2020 without infection and a control group of healthy normoacoustic subjects. RESULTS: The normality range was 4,16 ± 0,62 cps. 330 cases admitted for COVID-19 were evaluated from February 24th, 2020 to March 24th, 2021, 85 of them attended in ICU. After anamnesis and Audiometric Tone Thresholds developed as soon as possible, 9 SD were detected, all belonging to ICU group. The mean BV was 4,38 ± 0,43 cps in the ward group, 4,53 ± 0,39 cps in the ICU patients without SD, and 4,85 ± 0,52 cps in the cases with SD, with statistically significant differences. Highest BV elevations in the SD cases were detected between days 6 and 10 of hospital admission. In 2019 four cases consulted with SD, and another two did it in 2020 without a diagnosis of COVID-19, with normal BV values. CONCLUSIONS: During SARS-Cov-2 infection, patients may show high BV and SS, although an inpatients control group and a larger sample volume are necessary to confirm the predisposition to hyperviscosity. The incidence of hearing damage is considerable if its possible appearance is taken into account, within the limitations of critical patients with COVID-19.

Prone Positioning as a Potential Risk Factor for Deep Vein Thrombosis in COVID-19 Patients: A Hypothesis Generating Observation.

AIMS OF THE STUDY: Virchow's triad with stasis, activated coagulation, and endothelial damage is common in SARS-CoV2. Therefore, we sought to retrospectively assess whether the duration of prone position may serve as a risk factor for deep vein thrombosis in critically ill patients. METHODS: In this single center retrospective study of a tertiary referral hospital, patients with acute respiratory distress syndrome (ARDS) due to COVID-19 pneumonia admitted to critical care underwent venous ultrasound screening for deep vein thrombosis (DVT). Data on DVT diagnosis, duration of prone positioning, demographic, respiratory, and laboratory parameters were retrospectively collected and compared between DVT and non-DVT patients. RESULTS: 21 patients with ARDS from COVID-19 pneumonia were analyzed. DVT was detected in 11 (52%) patients (76.2% male, median age 64 (58; 68.5) years, median body mass index 31 (27; 33.8) kg/m2). In patients diagnosed with DVT, median prone ventilation had been maintained twice as long as compared to patients without DVT (57 (19; 72) versus 28 (0; 56.3) h, p = 0.227) on ICU day 5 with a trend towards longer prone position time (71 (19; 104) versus 28 (0; 73) h, p = 0.06) on ICU day 7. CONCLUSIONS: Prone ventilation and constitutional factors may constitute an additional risk factor for DVT in COVID-19 patients. Since recent studies have shown that therapeutic anticoagulation does not impact the occurrence of thromboembolic events, it may be worthwhile to consider mechanical factors potentially affecting blood flow stasis in this high-risk population. However, due to the limited number of patients, our observations should only be considered as hypothesis-generating. Future studies, sufficiently powered and preferably prospective, will be needed to confirm our hypothesis.

[Blood viscosity in COVID-19 patients with sudden deafness]. / Viscosidad sanguínea en pacientes COVID-19 con sordera súbita.

Background: Changes in blood viscoelastic properties have been proposed previosuly as etiopathogenesis for severe complications in COVID-19 and some cases of Sudden Deafness (SD). This is an attempt to verify if SD cases in patients admitted for SARS-CoV-2 infection can be correlated. Patients and methods: A prospective follow-up was carried out with COVID-19 patients, monitoring their blood viscosity (BV) at high shear rate (300 sec-1) and inquiring them periodically for eventual hearing loss. This measurement was extended to cases bearing of SD in 2019 and 2020 without infection and a control group of healthy normoacoustic subjects. Results: The normality range was 4,16±0,62 cps. 330 cases admitted for COVID-19 were evaluated from February 24th, 2020 to March 24th, 2021, 85 of them attended in ICU. After anamnesis and Audiometric Tone Thresholds developed as soon as possible, 9 SD were detected, all belonging to ICU group. The mean BV was 4,38±0,43 cps in the ward group, 4,53±0,39 cps in the ICU patients without SD, and 4,85±0,52 cps in the cases with SD, with statistically significant differences. Highest BV elevations in the SD cases were detected between days 6 and 10 of hospital admission. In 2019 four cases consulted with SD, and another two did it in 2020 without a diagnosis of COVID-19, with normal BV values. Conclusions: During SARS-CoV-2 infection, patients may show high BV and SS, although an inpatients control group and a larger sample volume are necessary to confirm the predisposition to hyperviscosity. The incidence of hearing damage is considerable if its possible appearance is taken into account, within the limitations of critical patients with COVID-19.