Position statement from the Indian Society of Gastroenterology, Cardiological Society of India, Indian Academy of Neurology and Vascular Society of India on gastrointestinal bleeding and endoscopic procedures in patients on antiplatelet and/or anticoagulant therapy.

Antiplatelet and/or anticoagulant agents (collectively known as antithrombotic agents) are used to reduce the risk of thromboembolic events in patients with conditions such as atrial fibrillation, acute coronary syndrome, recurrent stroke prevention, deep vein thrombosis, hypercoagulable states and endoprostheses. Antithrombotic-associated gastrointestinal (GI) bleeding is an increasing burden due to the growing population of advanced age with multiple comorbidities and the expanding indications for the use of antiplatelet agents and anticoagulants. GI bleeding in antithrombotic users is associated with an increase in short-term and long-term mortality. In addition, in recent decades, there has been an exponential increase in the use of diagnostic and therapeutic GI endoscopic procedures. Since endoscopic procedures hold an inherent risk of bleeding that depends on the type of endoscopy and patients' comorbidities, in patients already on antithrombotic therapies, the risk of procedure-related bleeding is further increased. Interrupting or modifying doses of these agents prior to any invasive procedures put these patients at increased risk of thromboembolic events. Although many international GI societies have published guidelines for the management of antithrombotic agents during an event of GI bleeding and during urgent and elective endoscopic procedures, no Indian guidelines exist that cater to Indian gastroenterologists and their patients. In this regard, the Indian Society of Gastroenterology (ISG), in association with the Cardiological Society of India (CSI), Indian Academy of Neurology (IAN) and Vascular Society of India (VSI), have developed a "Guidance Document" for the management of antithrombotic agents during an event of GI bleeding and during urgent and elective endoscopic procedures.

Decompressive surgery in cerebral venous sinus thrombosis due to vaccine-induced immune thrombotic thrombocytopenia.

BACKGROUND AND PURPOSE: Cerebral venous sinus thrombosis due to vaccine-induced immune thrombotic thrombocytopenia (CVST-VITT) is an adverse drug reaction occurring after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination. CVST-VITT patients often present with large intracerebral haemorrhages and a high proportion undergoes decompressive surgery. Clinical characteristics, therapeutic management and outcomes of CVST-VITT patients who underwent decompressive surgery are described and predictors of in-hospital mortality in these patients are explored. METHODS: Data from an ongoing international registry of patients who developed CVST within 28 days of SARS-CoV-2 vaccination, reported between 29 March 2021 and 10 May 2022, were used. Definite, probable and possible VITT cases, as defined by Pavord et al. (N Engl J Med 2021; 385: 1680-1689), were included. RESULTS: Decompressive surgery was performed in 34/128 (27%) patients with CVST-VITT. In-hospital mortality was 22/34 (65%) in the surgical and 27/94 (29%) in the non-surgical group (p < 0.001). In all surgical cases, the cause of death was brain herniation. The highest mortality rates were found amongst patients with preoperative coma (17/18, 94% vs. 4/14, 29% in the non-comatose; p < 0.001) and bilaterally absent pupillary reflexes (7/7, 100% vs. 6/9, 67% with unilaterally reactive pupil, and 4/11, 36% with bilaterally reactive pupils; p = 0.023). Postoperative imaging revealed worsening of index haemorrhagic lesion in 19 (70%) patients and new haemorrhagic lesions in 16 (59%) patients. At a median follow-up of 6 months, 8/10 of surgical CVST-VITT who survived admission were functionally independent. CONCLUSIONS: Almost two-thirds of surgical CVST-VITT patients died during hospital admission. Preoperative coma and bilateral absence of pupillary responses were associated with higher mortality rates. Survivors often achieved functional independence.

Eye signs for the neurologist in the Intensive Care Unit.

INTRODUCTION: The eyes are a window to the brain' is a maxim that holds true especially in the intensive care setting. Recognising specific eye signs aids rapid decision-making regarding diagnosis or prognosis. Eye signs play a pivotal role in intensive care for the neurologist. STATE OF THE ART: Eye signs have long been considered the best clinical clue for assessment of a comatose patient. In critically ill patients, the recognition of brainstem involvement hinges primarily on eye signs. The ability to recognise and interpret these signs goes a long way towards ensuring proper care of neurological illness in intensive care units. CLINICAL IMPLICATIONS: In this article we enumerate the various signs to be assessed in the ocular and periocular structures. We look at the various types of nystagmus and abnormal eye movements which help to localise lesions in the brainstem. This will aid better diagnosis and prognostication. We categorise eye signs as Category 1 or 2 according to whether they are periorbital and ocular signs or oculomotor abnormalities. Category 2 signs are further sub-classified into Category 2a - common and Category 2b - uncommon. FUTURE DIRECTIONS: Clinical anatomical correlation of specific signs such as ocular dipping has yet to be elucidated. Research that looks into specific eye signs may help with better anatomic correlation and localisation of lesions.

Causes of delayed arrival with acute ischemic stroke beyond the window period of thrombolysis.

CONTEXT: Early thrombolytic therapy in acute ischemic stroke has proven to reduce the associated morbidity. Many factors are in play, delaying the arrival of patients. AIM: To ascertain the factors causing delay in patients with acute ischemic stroke presenting beyond the window period of thrombolysis in and around Chennai, Tamil Nadu, India. SUBJECTS AND METHODS: An observational cross-sectional study involving 200 patients with acute ischemic stroke at Sri Ramachandra Medical College, Chennai, India between June 2015 and July 2016 was conducted. The data was collected by direct interview using a questionnaire designed to study factors such as age, family structure, residence, distance from the hospital, education status, wake-up stroke, transport, symptoms, knowledge about symptoms, seriousness of symptoms, waiting on symptoms, insurance and point of admission. Data was analyzed for means, frequencies, percentages and multiple linear regression analysis was performed to identify factors independently influencing delayed arrival. RESULTS: Mean age of the cohort was 58.08 years: 142 men and 58 women. Mean time of delayed arrival was 13.6 hours. Multiple linear regression analysis revealed that seriousness of symptoms (P = 0.001), residence (P = 0.001), point of admission (P = 0.033) and wake-up stroke (P = 0.005) were statistically significant predictors of delayed arrival. CONCLUSION: Patients not perceiving their symptoms to be serious, residing in a rural area, not arriving to the emergency, and having a stroke while awake were all the significant predictors of pre-hospital delay in our study. Awareness among the masses about symptom recognition and early arrival to a tertiary care center will reduce the delay and associated morbidity. Primary care physicians notably play a significant role in educating patients at risk, identifying the symptoms of stroke and referring them for thrombolysis.

Mystery of a cryptogenic stroke solved by an abdominal angiogram.

Despite advances in the field of imaging and diagnostics, the incidence of cryptogenic stroke is still around 30-40% in modern stroke databases. Our patient presented with recurrent midbrain infarcts over 3 years and was initially labelled as a patient with cryptogenic stroke. His blood investigations were normal, work up for autoimmune disorders was negative, CT brain angiogram was normal and a two-dimensional echo showed a small patent foramen ovale with a left to right shunt. He later presented with a right perinephric haematoma and an abdominal angiogram revealed multiple microaneurysms of the renal arteries, coeliac trunk and the mesenteric arterial system. The feeding renal artery was embolised. A diagnosis of polyarteritis nodosa was made. The patient was subjected to digital subtraction angiography of neck and intracranial vessels, which revealed multiple microaneurysms in internal and external carotid artery territory. He was discharged with steroids and azathioprine.