Epidural analgesia or anesthesia is a common procedure for pain relief, especially in obstetrics. Pneumorrhachis and pneumothorax are rare complications of epidural analgesia. They are considered asymptomatic entities but have recently caused increased morbidity and mortality. As the use of epidural analgesia and anesthesia increased significantly in the last decade, clinicians must be aware of this entity. This is a case report of pneumorrhachis causing pneumothorax and pneumomediastinum leading to respiratory distress. Case: A 26-year-old obese primigravida at 37 weeks’ gestation and with failure of progression of labor underwent lower segment cesarean section under epidural anesthesia. The procedure including the delivery of fetus was uneventful. In the post-anesthesia care unit, the patient became tachypneic, and her oxygen saturation was low despite supplemented oxygen by face mask and adequate analgesia. She was afebrile and was admitted to the surgical intensive care unit (SICU) for further management. In the SICU, incentive spirometry was initiated, and analgesia with intravenous fentanyl was given. Her echocardiogram was normal. Computer tomographic examination ruled out pulmonary embolism but showed pneumorrhachis with extension into the mediastinum and right apical pneumothorax. She was hemodynamically stable. In the next two days, her tachypnea settled, and the oxygen saturation improved to normal. On the third day, she was transferred to the ward and discharged home from there. She was followed up in the outpatient clinic after one and four weeks and was doing well, and her repeat imaging studies were normal. Conclusion: Epidural analgesia can lead to pneumorrhachis and can cause pneumothorax leading to respiratory distress.

Angiotensin converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) reduce cardiac remodelling, fibrosis, and inflammation. High-risk surgical patients requiring non-cardiac surgery are frequently prescribed ACEIs or ARBs as first-line therapy for hypertension and other conditions, including heart failure, myocardial infarction (MI) and stroke, diabetes mellitus leading to diabetic nephropathy, etc. However, the continuation of ACEIs or ARBs in the perioperative period has been associated with an increased risk of intraoperative hypotension. The data on the perioperative management of these medications are limited. Consider, a 73-years-old woman with hypertension and type 2 diabetes having bilateral salpingo-oophorectomy for ovarian cancer. Her medications included ramipril, amlodipine, and oral hypoglycaemic agents. The ramipril was continued perioperatively, and besides transient but severe hypotension at induction of anaesthesia, the patient's course was unremarkable. The present case-based review discusses the current controversies surrounding the perioperative management of ACEIs and ARBs.

Hydrocephalus (HCP) occurs due to the injurious effect of subarachnoid haemorrhage (SAH). It causes increased morbidity and mortality. It can be acute and frequently occurs within 48 hours and up to 7 days. Subacute hydrocephalus may occur up to 14 days and is chronic if remained or develops after 2 weeks of the subarachnoid haemorrhage. Acute hydrocephalus after aneurysmal subarachnoid (aSAH) bleeding is non-communicating or obstructive and occurs due to physical obstruction by a clot, the effect of blood in the subarachnoid space, and inflammation. Chronic hydrocephalus is due to fibrosis and adhesion, which hampers cerebrospinal fluid (CSF) absorption and increased secretion of CSF from gliosis. Various risk factors for developing hydrocephalus in aneurysmal subarachnoid haemorrhage patients range from female gender to high severity scores. Acute hydrocephalus frequently requires diversion drainage of CSF by external ventricular drain (EVD); it usually subsides within a week, and EVD is removed. Fewer patients will develop or continue to have hydrocephalus, requiring either short or longer shunting of the CSF namely by ventriculoperitoneal shunt or other modes of CSF drainage.

Background: Alzheimer’s disease (AD) is the leading neurodegenerative disorder affecting memory, learning and behavior. Altered expression of proteins involved in neuronal structure and function is a recent observation of AD pathogenesis. Modulation of altered protein expression seems promising in AD therapeutics. In the present experiment, AD ameliorating effect of medicinal mushroom Ganoderma lucidum had been evaluated through its effect on neuronal cytoskeletal structure and function related protein expression pattern in AD model rats. Methods: Wistar male rats (120 ± 5gm) were divided into three groups: control (C), AD (A) and G. lucidum hot water extract (HWE) fed AD (AE), each group containing 15 rats. AD model rats were prepared by infusing Aβ1-42 (ab120959, abcam, USA) into the cerebral ventricles. Protein extraction from the brain samples was performed following homogenization of the hippocampus (50 mg ) with lysis buffer (1ml) using a homogenizer (Polytron PT 1200, Kinematica). Protein separation through SDS-PAGE and protein quantification through LC-chip MS/MS Q-TOF had been performed for label-free relative quantification. For statistical analyses, the data were exported to the Mass Profiler Professional (MPP) software and ANOVA (P<0.05) had been performed to overcome the complications of false discovery associated with multiple test analyses. Functional interaction networks of the proteins were identified using the STRING (Search Tool for the Retrieval of Interacting Genes/Proteins) database (version 10.0; http://string-db.org/). For further identifying over-representing pathways and biological functions, the ingenuity pathway analysis (IPA), build version: 389077M, content version: 27821452, (Release date: 2016-06-14) was used (https://www.ingenuity.com/wp-content/themes/ingenuity-qiagen). Datasets of the proteins significantly expressed (P<0.05) and having log fold change of 1.5 and higher were uploaded (AD versus C, AD versus AE and C versus AE). Results: Among 2,212 proteins identified in the present study, 819 had been found to be differentially expressed. Of the differentially expressed ones, 9 proteins had been linked with neuronal cytoskeletal structure and function regulation such as tubulin, β-actin, dihydropyrimidinase-related protein 2 (DRP-2), keratin, glial fibrillary acidic protein (GFAP), Rho A proteins, septin, cofilin, gelsolin and dynamin. AD rats manifested altered expression of proteins associated with neuronal structure and function. G. lucidum hot water treatment ameliorated the altered expression of those proteins. Conclusions: Altered expression of hippocampal proteins is a hallmark of AD. Neuroproteomics regulatory approach towards AD amelioration seems promising. Inclusion of G. lucidum for proteomics based AD therapeutics in regulation of the proteins involved in neuronal structure and function seem apt. Thus, G. lucidum could be considered as an AD therapeutic agent.

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