The novel coronavirus (SARS-CoV-2) has turned into a life-threatening pandemic disease . About 5% of patients with Covid-19 have severe symptoms including septic shock, acute respiratory distress syndrome, and the failure of several organs, while most of them have mild symptoms. Frequently, the kidneys are involved through direct or indirect mechanisms. Kidney involvement mainly manifests itself as proteinuria and acute kidney injury (AKI). The SARS-CoV-2-induced kidney damage is expected to be multifactorial; directly it can infect the kidney podocytes and proximal tubular cells and based on an angiotensin-converting enzyme 2 (ACE2) pathway it can lead to acute tubular necrosis, protein leakage in Bowman's capsule, collapsing glomerulopathy and mitochondrial impairment. The SARS-CoV-2-driven dysregulation of the immune responses including cytokine storm, macrophage activation syndrome, and lymphopenia can be other causes of the AKI. Organ interactions, endothelial dysfunction, hypercoagulability, rhabdomyolysis, and sepsis are other potential mechanisms of AKI. Moreover, lower oxygen delivery to kidney may cause an ischaemic injury. Understanding the fundamental molecular pathways and pathophysiology of kidney injury and AKI in Covid-19 is necessary to develop management strategies and design effective therapies.

SummarySubclavian ‘steal’ phenomenon is a function of the proximal subclavian artery (SA) steno-occlusive disease, with subsequent retrograde blood flow in the ipsilateral vertebral artery (VA). The symptoms from the compromised vertebrobasilar and brachial blood flows constitute the subclavian steal syndrome (SSS), and include paroxysmal vertigo, drop attacks and/or arm claudication. Once thought to be rare, the emergence of new imaging techniques has drastically improved its diagnosis and prevalence. The syndrome, however, remains characteristically asymptomatic and solely poses no serious danger to the brain. Recent studies have shown a linear correlation between increasing arm blood pressure difference with the occurrence of symptoms. Atherosclerosis of the SA remains the most common cause. Doppler ultrasound is a useful screening tool, but the diagnosis must be confirmed by CT or MR angiography. Conservative treatment is the initial best therapy for this syndrome, with surgery reserved for refractory symptomatic cases. Percutaneous angioplasty and stenting, rather than bypass grafts of the subclavian artery, is the widely favored surgical approach. Nevertheless, large, prospective, randomized, controlled trials are needed to compare the long-term patency rates between the endovascular and open surgical techniques.

The available data are limited by low patient numbers, limited RCTs, and inconsistent methods between studies. However, a greater part of the data suggest that HTS given as either a bolus or continuous infusion can be more effective than mannitol in reducing episodes of elevated ICP. A meta-analysis of 8 prospective RCTs showed a higher rate of treatment failure or insufficiency with mannitol or normal saline versus HTS.

Vein of Galen aneurysmal malformations are a rare and diverse group of entities with a complex anatomy, pathophysiology, and serious clinical sequelae. Due to their complexity, there is no uniform treatment paradigm. Furthermore, treatment itself entails the risk of serious complication. Offering the best treatment option is dependent on an understanding of the aberrant anatomy and pathophysiology of these entities, and tailored therapy is recommended. Herein, the authors review the current concepts related to vein of Galen aneurysmal malformations and suggest a new classification system excluding mesodiencephalic plexiform intrinsic arteriovenous malformations from this group of malformations.

Anatomic knowledge of DL variations should aid the surgeon in repairing torn DLs.