Isquemia aguda por trombosis aórtica en COVID-19: A propósito de un caso

Objetivo: Presentar un caso de isquemia aguda por trombosis aórtica en paciente con infección por COVID-19 y exponer la importancia del diagnóstico y manejo oportuno. Introducción: El coronavirus (COVID-19) afecta principalmente al tracto respiratorio, pero presenta predisposición a fenómenos trombóticos y sus complicaciones, siendo una de las más graves la isquemia aguda por trombosis aórtica. Caso clínico: Paciente masculino de 68 años, que cursa con cuadro clínico de neumonía grave por COVID-19, presenta de forma concomitante episodio de trombosis aórtica aguda, resultando con isquemia aguda de extremidades inferiores. Se realizó trombectomía, post procedimiento y asociado a reperfusión, presentó paro cardiorrespiratorio con asistolia sostenida, falleciendo pese a maniobras de reanimación. Conclusión: Pese a las medidas de profilaxis con heparina de bajo peso molecular (HBPM), se deben sospechar y buscar las complicaciones tromboembólicas en pacientes que cursan con esta infección para dar un manejo oportuno y vigilar las complicaciones post quirúrgicas que pueden ser mortales.

Aim: To present a case of acute ischemia due to aortic thrombosis in a patient with COVID-19 infection and explain the importance of diagnosis and timely management. Introduction: The coronavirus (COVID-19) mainly affects the respiratory tract, but it has a predisposition to thrombotic phenomena and its complications, one of the most serious being acute ischemia due to aortic thrombosis. Clinical case: 68-year-old man, coronary heart disease with severe pneumonia due to COVID-19, presents aortic thrombosis, resulting in acute lower extremity ischemia. Thrombectomy was performed, post procedure and associated with reperfusion, presented cardiorespiratory arrest with sustained asystole, died despite resuscitation maneuvers. Conclusion: Despite prophylaxis measures with low molecular-weight heparins (LMWH), thromboembolic complications should be sought in patients with this infection to provide timely management and monitor post-surgical complications that can be fatal.

Surgical management of primary aortic thrombus in thoracic aorta.

Background: Primary aortic thrombus (PAT) in the absence of underlying aortic pathology such as atherosclerosis or aneurysm is quite rare and presents with various symptoms related to distal embolization. Treatment options include anticoagulation alone, open surgical thrombectomy, endovascular repair, and a combination of these approaches. The optimal management strategy remains controversial. Methods: Between 2016 and 2020, 10 patients (6 females; mean age, 49.1 years) presented to our institution with PAT in the thoracic aorta. All 10 patients were active tobacco users, and 6 patients were found to have an underlying hypercoagulable state. Locations of the PAT included the ascending aorta in 4 patients, the descending thoracic aorta in 3 patients, and the aortic root, aortic arch, and thoracoabdominal aorta in 1 patient each. At presentation, 2 patients had developed myocardial infarction, and 2 others had cerebral infarction. All patients but 1, who was managed medically for PAT, underwent open surgical thrombectomy via either sternotomy or left thoracotomy. Concomitant procedures included coronary artery bypass grafting in 2 patients and pulmonary thromboembolectomy in 1 patient. There were no operative deaths. During a median follow-up of 18 months, 2 patients developed recurrent PAT, owing primarily to poor compliance with anticoagulation. One patient required redo open thrombectomy. Two patients had mesenteric ischemia necessitating small bowel resection. Conclusions: Open surgical thrombectomy of the thoracic aorta can be performed with low mortality and morbidity; however, PAT can recur, especially in patients who have difficulty managing anticoagulation.

Acute superior mesenteric venous thrombosis results in high rates of readmission and morbidity.

OBJECTIVE: Superior mesenteric venous thrombosis (MVT) is a poorly understood clinical entity, and as such, outcomes are poorly described. This study aimed to identify predictors of bowel ischemia after MVT and to compare outcomes for patients treated medically (group 1) with those for patients treated with bowel resection (group 2). METHODS: This was a retrospective, single-institution study capturing all patients diagnosed with symptomatic acute MVT on computed tomography imaging from 2008 to 2018. Demographics, comorbidities, imaging, laboratory values, and treatment were included. Predictors of bowel resection were analyzed by univariate and multivariate statistics. Outcomes including mortality, readmissions for abdominal pain, and chronic mesenteric venous congestion were compared using χ2 test. RESULTS: There were 121 patients included in the study; 98 patients were treated medically (group 1), 19 patients were treated with bowel resection (group 2), and 4 patients were treated with endovascular recanalization (group 3). Group 1 and group 2 were compared directly. Patients requiring bowel resection tended to have higher body mass index (P = .051) and a hypercoagulable disorder (P = .003). Patients who required bowel resection were more likely to present with lactic acidosis (P < .001) and leukocytosis (P < .001) with bowel wall thickening on scan (P < .001). On multivariable analysis, a genetic thrombophilia was a strong predictor of bowel ischemia (odds ratio, 3.81; 95% confidence interval, 1.12-12.37). One-year mortality and readmission rates did not differ between groups. However, readmission rates for abdominal pain were high for both groups (group 1, 44.90%; group 2, 57.89%; P = .317), and a significant proportion of patients exhibited chronic mesenteric venous congestion on repeated scan (group 1, 42.86%; group 2, 47.37%; P = .104). CONCLUSIONS: A genetic hypercoagulable disorder is a predictor of bowel ischemia due to MVT. Regardless of treatment, outcomes after MVT are morbid, with high rates of readmission for abdominal pain. An alternative approach to treat these patients is needed, given the poor outcomes with current strategies.

Hepatitis C Virus Infection and Risk of Venous Thromboembolism: A Systematic Review and Meta-Analysis.

BACKGROUND/OBJECTIVES: Hepatitis C virus (HCV) infection is one of the leading causes of cirrhosis. As a result of chronic inflammatory response to the virus, HCV-infected patients may be at a higher risk of venous thromboembolism (VTE). However, the data on this association is unclear. This systematic review and meta-analysis was conducted with the aims to summarize all available evidence. MATERIAL AND METHODS: A literature search was performed using MEDLINE and EMBASE from inception to April 2016. Studies that reported relative risks, odd ratios, or hazard ratios comparing the risk of VTE among HCV-infected patients vs. subjects without HCV infection were included. Pooled risk ratios (RR) and 95% confidence interval (CI) were calculated using a random-effect, generic inverse variance method. RESULTS: Three studies met our eligibility criteria and were included in analysis. The pooled RR of VTE in HCV-infected patients vs. subjects without HCV infection was 1.38 (95% CI, 1.08-1.77, I2 = 40%). Subgroup analysis showed that risk was increased for both pulmonary embolism (PE) and deep venous thrombosis (DVT) even though without adequate power to demonstrate statistical significance (Pooled RR of 1.34, 95% CI, 0.67-2.66 for PE and pooled RR 1.45, 95% CI, 0.93-2.77 for DVT). CONCLUSION: Our study demonstrated a significantly increased risk of VTE among HCV-infected patients. Further studies are required to clarify how this risk should be addressed in clinical practice.

Trombosis de senos venosos cerebrales, una manifestación inusual de déficit de proteína S en paciente joven / Cerebral venous sinus thrombosis, an unusual manifestation of protein s deficiency in young patients

Resumen La trombosis venosa cerebral (TSVC) es un tipo de accidente cerebrovascular (ACV) que involucra el lado venoso de la circulación cerebral, incluye trombosis de los senos venosos durales y/o de las venas corticales y profundas del cerebro, es una causa poco común 0,5-1 % de todos los accidentes cerebrovasculares, con una prevalencia estimada en el rango entre 0. 22 a 1,23 / 100.000 / año. Los factores de riesgo para TSVC, están generalmente divididos en riesgos adquiridos (por ejemplo: cirugía, trauma, embarazo, puerperio, síndrome antifosfolípido, cáncer, hormonas exógenas) y los riesgos genéticos (trombofilia hereditaria). Los factores de riesgo más ampliamente estudiados para TSVC incluyen estados protrombóticos, las trombofilias heredadas asociadas con TSVC incluyen deficiencias de antitrombina, proteína C, proteína S (PS), mutación del factor V Leiden y la mutación del gen 20210 de protrombina. La prevalencia del déficit de PS, oscila entre un 0,02 y un 0,03 % en la población general y aumenta hasta un 2 % en pacientes no seleccionados con trombosis. Con una mortalidad cercana al 9 %. El manejo es usualmente médico. Se cita el caso de una paciente de 28 años de edad, con cuadro clínico de cefalea de 1 mes de evolución, con hallazgos en neuroimagen de trombosis de senos transverso y sigmoideo izquierdo con déficit de proteína S.

Summary Cerebral venous thrombosis (TSVC) is a type of stroke (CVA) involving the venous side of the cerebral circulation, including thrombosis of the dural venous sinuses and / or cortical and deep veins of the brain, is a rare cause 0.5-1% of all strokes, with an estimated range between 0. 22 to 1.23 / 100,000 / year prevalence. Risk factors for TSVC, are generally divided into acquired risks (eg, surgery, trauma, pregnancy, postpartum, antiphospholipid syndrome, cancer, exogenous hormones) and genetic risks (hereditary thrombophilia). The most widely studied factors TSVC risk include prothrombotic states, inherited thrombophilia associated with deficiencies TSVC include antithrombin, protein C, protein S (PS), mutation of factor V Leiden mutation and prothrombin 20210 gene. The prevalence of PS deficit ranges between 0.02 and 0.03% in the general population and increases up to 2% in unselected patients with thrombosis. With close to 9% mortality. The operation is usually doctor. It cites the case of a 28-year-old, with clinical symptoms of headache 1 month of evolution with neuroimaging findings transverse sinus thrombosis and left sigmoid with protein S deficiency.

Coagulation Profile Dynamics in Pediatric Patients with Cushing Syndrome: A Prospective, Observational Comparative Study.

OBJECTIVE: To evaluate the association between Cushing syndrome and hypercoagulability in children. STUDY DESIGN: A prospective, observational study was performed of 54 patients with Cushing syndrome, 15.1 ± 3.9 years, treated at the National Institutes of Health Clinical Center. Coagulation profiles were taken before and 6-12 months after surgery and compared with18 normocortisolemic children, 13.7 ± 3.6 years. RESULTS: At baseline, patients with Cushing syndrome had greater levels of the procoagulant factor VIII (FVIII) vs controls (145 IU/dL ± 84 vs 99 ± 47, P = .04); 6-12 months after surgery, FVIII levels decreased to 111 ± 47, P = .05. Patients with Cushing syndrome had greater levels of the antifibrinolytic α2-antiplasmin, 96 ± 17% vs 82 ± 26%, P = .015. After surgery, antifibrinolytic α2-antiplasmin levels decreased to 82 ± 24%, P < .001. Anticoagulants were greater in patients with Cushing syndrome vs controls at baseline, including protein C (138 ± 41% vs 84 ± 25%, P < .001), protein S (94 ± 19% vs 74 ± 19%, P = .001), and antithrombin III (96 ± 18% vs 77 ± 13%, P < .0001). The 24-hour urinary free cortisol levels correlated positively with FVIII levels, r = 0.43, P = .004. CONCLUSION: Children with Cushing syndrome had elevated procoagulants, antifibrinolytics, and anticoagulants at baseline compared with controls; normalization of coagulation measures was seen after surgical cure. Despite the increase in anticoagulants, hypercortisolemia is associated with a hypercoagulable state in children, as is the case in adults. This finding has potential implications for prevention of venous thromboembolism in children with Cushing syndrome. TRIAL REGISTRATION: ClinicalTrials.gov:NCT00001595.