Concurrent pulmonary arteriovenous malformation and pulmonary embolism causing stroke: a therapeutic dilemma

Background As pulmonary arteriovenous malformation (PAVM) include a right-to-left shunt, it can be accompanied by fatal complications such as stroke and brain abscess due to paradoxical embolism. A concurrent PAVM and pulmonary embolism (PE) is a rare condition. Therefore, the sequence of management has not been established. Case presentation A 62-year-old female patient was transferred to our hospital with a sporadic simple PAVM and concurrent bilateral PE. On chest computed tomography (CT), the acute PE was extended to the segmental pulmonary artery where the feeding artery of PAVM originated. Despite the anticoagulation, the patient complained of left sided weakness on the fifth day of admission, and magnetic resonance imaging revealed an acute infarction in the right lateral thalamus, which was thought to be caused by paradoxical embolism. This situation could lead to a dilemma between the risk of thrombus migration during PAVM embolization and another embolic event due to delayed shunt occlusion during anticoagulation. After a multidisciplinary discussion, a delayed endovascular embolization was performed for PAVM after confirming the complete resolution of PE with 4 months of anticoagulation. The cause of PE in this patient was eventually diagnosed as antiphospholipid syndrome. Conclusion The authors reported a rare case of concurrent PAVM and PE that led to an embolic stroke during hospitalization. This patient was managed with delayed endovascular embolization for PAVM after an anticoagulation for PE and stroke. It is thought to be valuable in deciding for a treatment plan for this rare condition.

A case of recurrent cavernous sinus dural arteriovenous fistula arising after superselective shunt occlusion and detected by venous arterial spin labeling

Background: Superselective shunt occlusion (SSSO) for cavernous sinus dural arteriovenous fistula (CSDAVF) avoids the risk of cranial nerve palsy, unlike entire sinus packing, but requires paying attention to recurrence. Distinguishing between true and paradoxical worsening of postoperative ophthalmic symptoms using a less-invasive modality is often difficult. Here, we report a case of true worsening of neuro-ophthalmic symptom by recurrent CSDAVF detected by venous-arterial spin labeling (ASL) on magnetic resonance imaging. Case Description: A 55-year-old woman with neither contributory medical history nor previous head trauma presented with neuro-ophthalmic symptoms and pulsatile tinnitus. Digital subtraction angiography (DSA) revealed CSDAVF with multiple shunted pouches. She underwent successful transvenous SSSO, but neuroophthalmic symptom worsened after SSSO and venous-ASL revealed increased signal intensity in the right superior orbital vein (SOV). DSA confirmed recurrent CSDAVF and additional transvenous embolization was performed. Neuro-ophthalmic symptoms and venous-ASL hyperintensity on SOV improved postoperatively. Conclusion: Venous-ASL is noninvasive and seems useful for detecting true worsening of neuro-ophthalmic symptoms of recurrent CSDAVF.

The influence of metabolic activity of platelets on sensitivity to Acetylsalicylic acid in patients with coronary heart disease

Background Acetylsalicylic acid (ASA) is used to reduce the risk of shunt occlusion after coronary artery bypass grafting (CABG). From 5% to 60% of CHD patients do not respond to ASA. This phenomenon was defined as ASA resistance. The functional activity of platelets is largely determined by the state of their metabolism. Methods The venous blood samples were acquired from 66 patients with CHD before CABG, on the first day after surgery, and on the 8–10th day after surgery. The aggregometry was carried out for all participants by an optical aggregometer with 1 mM of arachidonic acid (AA) and 5 mM Adenosinediphosphate (ADP). Resistance to ASA was determined at the level of platelet aggregation with AA over 20% on ASA therapy or over 20% after platelet incubation with ASA in vitro before CABG. Patients were divided into ASA sensitive (sASA) and ASA resistant (rASA) groups. The level of synthesis of primary and secondary reactive oxygen species (ROS) by platelets was determined using chemiluminescent analysis. We investigated the overall level of radical synthesis from the values of Imax and S (area under the chemiluminescence curve), which, respectively, characterizes the maximum synthesis per unit time and the total amount of radical. The kinetics of ROS synthesis was characterized by Tmax (time to reach the maximum for the chemiluminescent curve). The activity of NAD- and NADP-dependent dehydrogenases in platelets was determined by the bioluminescent method. Results It was found that the aggregation activity of platelets depended on the sensitivity of CHD patients to ASA and decreased during postoperative ASA therapy. The most pronounced differences in metabolic parameters of platelets in sASA and rASA patients were detected by Nox2 activity. Platelet aggregation activity was correlated with platelet Nox2 activity only in sASA patients and only before CABG. The level of AA-induced platelet aggregation with the addition of ASA in sASA patients before CABG was negatively correlated with the Imax of ADP-induced lucigenin-enhanced (r=−0.27, p=0.046) and S of spontaneous luminol-enhanced (r=−0.31, p=0.022) platelet chemiluminescence. Patients with rASA before CABG had positive correlations of AA-induced aggregation with S of spontaneous (r=0.63, p=0.029) as well as Imax (r=0.85, p<0.001) and S (r=0.87, p<0.001) of ADP-induced luminol-enhanced chemiluminescence of platelets. Therefore, the absence of correlations between platelet aggregation activity and Nox2 activity was determined by ASA resistance and postoperative ASA therapy. The synthesis of secondary ROS (Table) by platelets of CHD patients did not depend on the sensitivity of patients to ASA but increased during postoperative treatment with ASA. The activity of NAD(P)-dependent dehydrogenases in platelets did not differ in sASA and rASA patients with CHD. Conclusions Metabolic Activity of Platelets could influence on resistance to ASA in Patients with CHD. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The reported study was funded by Russian Foundation for Basic Research, Government of Krasno-yarsk Territory, Krasnoyarsk Regional Fund of Science to the research project: “Antiplatelet therapy personification in patients with coronary heart disease (CHD) depending on the level of P-selectin gene expression, the intensity of intercellular interaction and inflammation”

Shunt coronarography in patients with recurrent stenocardia in long term after aorto-coronary bypass

Проблема профилактики и диагностики стеноза - окклюзирования шунтов после аорто - коронарного шунтирования в отдаленном периоде остается нерешенной. Наиболее часто закрываются шунты в течение первого года, возникновение окклюзии венозных шунтов в течение первого года после операции наблюдаются у 25-30% больных, в дальнейшем в течении 5-7 лет частота окклюзии составляет около 2% в год, после этого срока 5% в год. Артериальные шунты остаются проходимы до 98%, и в основном причиной их дисфункции является прогрессирование атеросклеротического процесса и технические погрешности. Основными причинами которые могут привести к нарушению функции шунта в отдаленном периоде считают [1, 2, 4, 6, 8] следующие: 1-техническое (повреждение эндотелиального слоя и стенки аутовенозного трансплантата при его взятии (ретроспективный анализ), чрезмерная длина и перегиб шунта (на шунтографии), натяжение шунта из-за недостаточной его длины, неправильный выбор места наложения дистального анастомоза) [11,12,13]. 2- анатомические факторы[3, 5, 7] . 3 - общие факторы (низкая объемная скорость кровотока по шунту, нестабильность общей гемодинамики, массивные сращения в полости перикарда, гиперкоагуляция, гнойный медиастинит, длительное лихорадочное состояние и неадекватный прием антикоагулянтов. 4 - прогрессирование атеросклероза [9]. 5- использование венозных трансплантантов как одна из важных причин стеноза - окклюзии шунта [10]. The Problem of stenosis prevention and diagnostics - occlusion of shunts after aorto-coronary bypass in long term remains unaddressed. Typically, shunts are closed within the first year, emergence of phleboid shunts occlusion within the first year after surgical intervention is observed in 25-30% of patients, and further frequency of occlusion within 5-7 years is about 2% per year, 5% per year after this term. Arterial shunts is passable up to 98%, and mainly the reason for their dysfunction is the atherosclerotic process progression and technical faults. The main reasons which can results in shunt dysfunction in long term are the following [1, 2, 4, 6, 8]: 1-technical (damage of endothelial layer and paries of autovenous transplant during its drawing (retrospective analysis), excess length and shunt bend (at the shuntography), shunt tension because of its insufficient length, improper location of distal anastomosis application) [11,12,13]. 2- anatomical factors [3, 5, 7] . 3 - general factors (low volumetric blood flow along the shunt, instability of general hemodynamics, dense adhesion in pericardial cavity, hypercoagulability, purulent mediastinitis, prolonged febrile state and inadequate intake of anticoagulants. 4 - atherosclerosis prgression [9]. 5- using venous transplants as one of the important reasons of stenosis - shunt occlusion [10].

Shunt occlusion in neonates with congenital heart disease undergoing systemic-to-pulmonary shunt surgery in the Neonatal Intensive Care Unit, Maharaj Nakorn Chiang Mai Hospital

Objectives To study occlusion of shunts and related factors in neonates after systemic-to-pulmonary shunt surgery. Methods This retrospective descriptive study reviewed the medical records of neonates in the Neonatal Intensive Care Unit who underwent a systemic-to-pulmonary shunt operation at Maharaj Nakorn Chiang Mai Hospital between January 1, 2011 and December 31, 2016. Patient characteristics and operative data were collected. Demographic data and incidence of shunt occlusion were analyzed using descriptive statistics. Factors associated with shunt occlusion were identified using Fisher’s exact test and the Mann-Whitney U test. Results Seventy-five newborns were enrolled in the study, of whom 39 (52.0%) were female. The average birth weight was 2,711.1 grams, and the average gestational age was 37.6 weeks. The number of newborns with TOF or TOF/IVS was equal to those with PA/IVS (34.7%). Sixty neonates (80%) underwent Modified Blalock Taussig shunt surgery, most (57.3%) with a 3.5 Fr. diameter shunt. The average weight at surgery was 2,898.9 grams, and the average age at surgery was 17.6 days. Anticoagulant and anti-platelet medication was used with almost all the neonates following surgery (96.0% and 93.3%, respectively). The incidence of shunt occlusion was 22.7% (17 neonates). Complete occlusion was found in 11 neonates. In-hospital shunt occlusion occurred in 10 neonates as well as in 7 neonates after discharge from the hospital. The overall mortality rate was 14.7%. Congenital heart disease diagnosis and gestational age were significantly associated with shunt occlusion (p = 0.02 and p = 0.01, respectively). Conclusion The study results can be used to provide develop guidelines for treatment of neonates with complex heart disease and low gestational age as well as nursing care guidelines for the prevention of blockage of the shunt in neonates undergoing a systemic-to-pulmonary shunt operation due to hospitalization in a hospital.

Sinking Skin Flap Syndrome following Posttraumatic Hydrocephalus

Introduction. Complications following craniotomy are not uncommon and Sinking Skin Flap Syndrome (SSFS) constitutes a rare entity that may present after a large Decompressive Craniectomy. Although the entity is widely reported, the literature mostly consists of case reports. Authors present a case series of three patients with review of literature highlighting the various factors which can prove therapeutic and can help in avoidance of complications. Materials and Methods. The study was conducted over a period of 3 years, from 2016 to 2019, and included 212 patients who underwent unilateral Decompressive Craniectomy (DC) for trauma in our institute. All 212 patients underwent a similar DC following a strict institutional protocol and the craniectomies were performed by the same surgical team. At total of 160 patients survived and elective cranioplasty was planned at a 3-month interval. Out of a total of 160 patients who survived, 38 developed hydrocephalus, 3 patients presented with hydrocephalus acutely and had to be shunted before cranioplasty and underwent ventriculoperitoneal (VP) shunting on the opposite side of craniectomy. All 3 of these patients developed SSFS and were the focus of this case series wherein review of literature was done with emphasis being laid on the salient features towards management of SSFS in such precranioplasty shunted patients. These 3 patients were treated via rehydration using normal saline (NS) till the Central Venous Pressure (CVP) equaled 8–10 cm of water, nursing in Trendelenburg position and shunt occlusion using silk 3-0 round bodied suture tied over a “C”-loop of VP shunt tube over clavicle. This was followed by cranioplasty within 2 days of presentation using a flattened, nonconvex artificial Polymethyl Methacrylate (PMMA) bone flap with central hitch suture taken across the bone flap and release of shunt tie in immediate postoperative period. The PMMA bone flap was made intraoperatively after measuring the defect size accurately after exposure of defect. 3D printing option was not availed by any patient considering the high cost and patients’ poor socioeconomic status. Results. Out of a total of 212 patients, thirty-eight patients (19%) developed posttraumatic hydrocephalus and out of 38, three presented with SSFS over the course of time. Two patients presented with hemiparesis of the side opposite to sunken flap while 1 other patient was brought by relatives in stuporous state. All 3 were subjected to VP shunt tie, rehydration, and cranioplasty using flattened artificial bone flap and showed gradual recovery in postoperative period without any complications. Conclusion. Various factors like nursing in Trendelenburg position, adequate rehydration, early cranioplasty after resolution of oedema, preoperative tying of VP shunt and its subsequent release in immediate postoperative period, use of flattened PMMA bone flaps, placement of a central dural hitch suture across the bone, and a preoperative central burr hole in the bone flap may accelerate healing and, in most cases, reversal of sensory-motor deficits along with reduction in complication rates.

Congenital portosystemic shunt occlusion with an Amplatzer PFO occlusion device: a case report

Background Congenital portosystemic shunts are embryological malformations in which portal venous flow is diverted to the systemic circulation. High morbidity and mortality are seen in patients with concurrent hepatic encephalopathy, hepatopulmonary syndrome, and pulmonary hypertension. Endovascular therapy, in the correct patient population, offers a less invasive method of treatment with rapid relief of symptoms. Case presentation In this report, we discuss the treatment of a two-year-old male with abnormal chorea-like movements, altered mental status, anisocoria and hyperammonemia diagnosed with an intrahepatic congenital portosystemic shunt between the inferior vena cava and right portal vein. Given the patient’s amenable anatomy and shunt type, embolization was performed with an 18 mm Amplatzer patent foramen ovale occlusion device. Conclusions Portosystemic shunts are a rare congenital abnormality without universal treatment guidelines. An Amplatzer PFO occlusion device can provide a novel method of shunt closure given appropriate shunt type, size and anatomy.

Modelling fluid and particulate flow through a ventriculoperitoneal shunt in a variable temperature environment

One of the most prevalent causes of failure for a ventriculoperitoneal shunt is blockage, the other being infection. This study looks at the blockage of the shunt valve, and whether the occlusion of a shunt valve is accelerated by the presence of an infection. This study assumes that an infection will raise the number of white blood cells contained in the cerebrospinal fluid to fight it and will thus accelerate shunt occlusion. The experiment simulates a shunt system by suspending a shunt valve in a water bath that has a temperature that varies between 37°C and 41°C. A computational fluid dynamics model of the shunt system is used to gain further insight into the flow behaviour under these conditions. The results of the CFD model were validated using the experimental results. There was an average error of 15% between the readings that were obtained in the experiment and the CFD model. The experimental results showed that there was a decrease in the volume flow rate at the outlet of the shunt system, which was not large enough to point towards any blockage. Both the model predictions and the experimental results show that increased temperature and particulate concentration alone do not result in shunt occlusion, particularly at the shunt valve. This result effectively excluded the shunt valve as a region of shunt occlusion due to infection, as an infection occurs due to the growth of bacteria along the surfaces of the shunt system and this bacterial growth is more likely to occur at the proximal and distal ends of the shunt system.

Multidisciplinary approach to the complex treatment for non-cirrhotic portal hypertension – case-report-based discussion

Non-cirrhotic portal vein thrombosis (PVT) in patients with antiphospholipid syndrome (APS) is a rare complication, and the management has to be determined individually based on the extent and severity of the presentation. We report on a 37-year-old male patient with non-cirrhotic chronic PVT related to a severe thrombophilia, comprising APS, antithrombin-, factor V- and factor X-deficiency. Three years after the initial diagnosis of non-cirrhotic PVT, the patient presented with severe hemorrhagic shock related to acute bleeding from esophageal varices, requiring an emergency transjugular intrahepatic portosystemic stent shunt (TIPSS). TIPSS was revised after a recurrent bleeding episode due to insufficient reduction of the portal pressure. Additionally, embolization of the dilated V. coronaria ventriculi led to the regression of esophageal varices but resulted simultaneously in a left-sided portal hypertension (LSPH) with development of stomach wall and perisplenic varices. After a third episode of acute esophageal varices bleeding, a surgical distal splenorenal shunt (Warren shunt) was performed to reduce the LSPH. Despite anticoagulation with low molecular weight heparin and antithrombin substitution, endoluminal thrombosis led to a complete Warren shunt occlusion, aggravating the severe splenomegaly and pancytopenia. Finally, a partial spleen embolization (PSE) was performed. In the postinterventional course, leukocyte and platelet counts increased rapidly and the patient showed no further bleeding episodes. Overall, this complex course demonstrates the need for individual assessment of multimodal treatment options in non-cirrhotic portal hypertension. This young patient required triple modality porto-systemic pressure reduction (TIPSS, Warren shunt, PSE) and involved finely balanced anticoagulation and bleeding control.