Trichosporon asahii is a rare opportunistic fungal pathogen that causes fatal systemic infection in immunocompromised patients. Neutropenia developing due to malignancies is an important risk factor for fungal infection. Invasive infections due to T. asahii can be divided into disseminated and localized forms. The disseminated form is more common and usually occurs in neutropenic patients. The patient typically has an acute febrile illness that progresses rapidly to multiorgan failure. Here, we are presenting a case of fungal sepsis by invasive T. asahii in a 1-year-old child with Wilms Tumor. To the best of our knowledge, this is the first time that fungal sepsis due to T. asahii has been reported in a Wilms tumor patient. The incidence of rare invasive fungal infections is increasing in immunocompromised patients in whom management becomes difficult due to their heterogenous antifungal susceptibility pattern and intrinsic resistance to the standard antifungal agents that are routinely given. The patient was admitted with high spiking fever, and his laboratory investigations suggested neutropenia. T. asahii was isolated from the blood culture, for which he was started on inj. voriconozole. After 14 days of treatment, the fungus was cleared out from the patient’s blood.

Background: As known to every Neuroscientist the spontaneous subarachnoid haemorrhage is a medical condition in which bleeding occurs in subarachnoid space due to cerebrovascular disease most commonly due ruptured aneurysms. Nimodipine is a calcium channel antagonist used to treat vasospasm. When compared to oral, intravenous nimodipine shows better neurological outcome with low dose, less frequency of administration and less fluctuations of blood pressure in between doses ( as in oral ) due to availability of continuous infusion . Titrated dose Intra venous nimodipine is useful in the initial Intensive Care management of Subarachnoid haemorrhage for Vasospasm with close monitoring of blood pressure.Objective: To evaluate the clinical outcomes of intravenous Nimodipine in the management of acute ischemic vasospasm in subarachnoid hemorrhagic patients. Material and methods: The study was a prospective and observational study conducted in all inpatients with SAH having acute ischemic vasospasm in the intensive care unit using IV Nimodipine admitted the department of Neurosurgery in AIMS during a period of 1yr.Results: Evaluation of SAH occurrence in study patients (n=38) showed predominance of females (68.4%) and majority with hypertension (57.9%) as the common comorbid condition. The chance of developing SAH was high in patients who did not practice any form of exercise (60.5%). None of the patients had occurrence of adverse drug reactions while administering IV nimodipine other than hypotension which was corrected with inotropic support with close blood pressure monitoring. Out of the subjects enrolled, 37 patients showed improvement clinically and resolution of ischemic changes in CT scan . Majority of patients experienced cerebral edema. Using pair t test, it was found that the difference between the Glasgow Coma Score pre and follow up post treatment score were mild. Using pair t test, it was found that the difference between the mRS pre and follow up post treatment score were significant.Conclusion: Introduction of IV Nimodipine to the treatment strategy of SAH showed significant improvement in the clinical and radiological outcome.IV Nimodipine showed benefit in treating the condition without any life-threatening adverse events other than correctable hypotension. A significant decrease in the mRS score in majority of patients after treatment indicates the improvement in the quality of life of SAH patients. Pre and Post neurological status strengthens the evidence of improvement in our study subjects.

The COVID-19 pandemic has overwhelmed our health care capacity in an unprecedented way due to the sheer number of critically infected patients admitted to hospitals during the last two years. Endothelial injury is seen as one of the central hallmarks of COVID-19 infection that is the starting point in the generation of microthrombi and sepsis eventually leading to acute respiratory distress syndrome (ARDs) and multi-organ failure. The dramatic fall in lung function during ARDs is attributed to the microthrombi-induced coagulopathy primed by a hyperactive immune system. Due to the lack of effective antiviral agents, the line of treatment is limited to the management of two key risk factors i.e., immune activation and coagulopathy. In the present review, we describe the mechanistic role, therapeutic targets and opportunities to control immune activation and coagulopathy during the pathogenesis of COVID-19-induced ARDs.

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