Background: CNS neoplasms are a heterogenous group contributing to <2% of all the malignant neoplasms. Imaging and histopathology play a great role in diagnosing these lesions. Aim of the study is to correlate radiological findings with that of histopathology and evaluate the role of Ki 67 proliferative index in various grades of Astrocytomas and MeningiomasMethods: This is an observational study for a period 2 years from July 2015 to June 2017 in Department of Pathology Andhra Medical College. The total number of specimens of CNS tumors received during this period were126. The specimens were routinely processed and stained with H&E. The tumors were classified based on WHO 2016 classification. In total 71 cases-45 cases of meningiomas and 26 cases of astrocytomas, the expression of Ki 67 labelling index was recorded in various grades of these tumors and results tabulated.Results: Among 126 cases, tumors predominantly encountered were of meningeal origin accounting to 45 cases (35.71%) followed by tumors of neuroepithelial origin 35 cases (27.78%). Tumors were seen in all age groups, but common was among 41-50 years of age group with metastatic tumors being seen in >60 year group. Tumors were more common in males with male: female ratio being 1.25:1. Ki 67 proliferative index increased as the grade of tumor increased in both astrocytomas and meningiomas.Conclusions: Grading of meningiomas and astrocytomas are very much essential with reference to prognosis and therapy. Histopathology plays a great role in grading these lesions but Ki 67 proliferative index adds as an adjunct and helps in confirmation and predicting the recurrence of these lesions.

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A case of pulmonary embolism in which the diagnosis was aided by transthorasic echocardiography is described. Echocardiography may be helpful in emergency presentations, as ECG changes can be neither sensitive nor specific for the diagnosis of acute massive pulmonary embolism.A 25 year old man presented with a 1 week history of non-productive cough and shortness of breath on exertion. Over the preceding month, he had experienced intermittent palpitations on several occasions. He had received antibiotics from his general practitioner for cellulitis in the left leg. There was no history of chest pain or haemoptysis. Past medical history was of mild asthma. There was no significant family history of medical problems. He was a non-smoker and occasionally drank alcohol.Examination revealed a moderately built man, who was apyrexial, tachypnoeic, and tachycardic, but not in respiratory distress. Blood pressure was 135/85, pulse regular and 110 beats/min, respiration rate 20 breaths/min, O 2 saturation 94% (on 2 litres of O 2 ). Chest auscultation revealed a loud second heart sound. An ejection systolic murmur was heard at the left sternal edge radiating to the neck. The chest was clear. There was minimal oedema of the left leg, with a swollen but non-tender calf. There were no abnormal abdominal or CNS findings.Blood results were: haemoglobin 16 g/l, white cell count 14.4610 9 /l, platelets 226610 9 /l, D-dimer 2 U (normal range 0-0.5). Troponin T and thrombophilia screens were negative. Arterial blood gases showed PO 2 of 10 kPa, PCO 2 of 3.9 kPa, and pH of 7.42. Chest x ray revealed enlarged pulmonary arteries, and ECG showed left axis deviation and anteroseptal ST/T depression (fig 1).A diagnosis of pulmonary embolism (PE) was made and anticoagulation with tinzaparin was initiated, followed by warfarin treatment. An early transthoracic echocardiogram revealed dilated right heart chambers with good left and right ventricle function and mild to moderate tricuspid regurgitation with estimated pulmonary artery systolic pressure of 68 mmHg. There was paradoxical septal motion due to right heart dilatation. A subsequent V/Q scan detected a number of significant unmatched perfusion defects in the left lung and one on the right, suggesting a high probability of PE.The patient made a good recovery and was allowed home with continuing warfarin treatment. DISCUSSIONThis case highlights the value of early echocardiogram in the diagnosis of acute massive PE. PE is both underdiagnosed and overdiagnosed. Acute PE causes up to 10% of all hospital deaths, with most occurring because of a delay in diagnosis, as PE is easily missed in elderly patients, patients with cardiorespiratory disease, and those presenting with isolated dyspnoea. A high index of suspicion is required to achieve an accurate diagnosis.Most ECG features in PE lack specificity and sensitivity, and the value of ECG for the diagnosis of PE is debatable. ECG can be normal in pulmonary embolism, and other recognised features of include sinus tachycardia (heart rate .10...