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Washington University Experience | NEOPLASMS (GLIAL) | Glioblastoma - Gross Pathology | 26A0 Case 26 History
Case 26 History ---- The patient was a 53 year old right handed male who expired 15 months following onset of symptoms related to a left parietal GBM which was treated with surgery, radiation therapy, and chemotherapy. In August of 1978 at age 52 he was noted to have the sudden onset of dysphasia which was followed by a generalized convulsion. CT scan and EEG were normal. He gradually improved and was able to return to his job as a maintenance foreman. In October of 1978 a similar episode occurred. A CT scan and cerebral arteriogram were interpreted as normal at that time. Two more episodes occurred in December 1978 and January 1979; CT scan was interpreted as showing a left parietal infarct with arteriography showing low flow to the left parietal region, interpreted as an infarct. After a left-sided headache and right arm weakness developed in March 1979, he was admitted to BJH. A CT scan showed a large left parietal mass, with irregular contrast enhancement, and a midline shift. In 3/1979 a left parietal craniotomy was performed with limited resection of a glioblastoma. Due to continued deterioration with increasing right hemiparesis, aphasia, and increased size of the mass on CT scan, a second craniotomy was performed in 4/79 with an excision of a large amount of tumor. Radiation therapy was given at a dose of 5,000 rads over 5 weeks’ time. Due to progressive right paresis involving the leg and the appearance of a right homonymous hemianopsia, the patient was treated with high dose BCNU with autologous bone marrow rescue. In August 1979. CT scan 6 weeks later showed diminished size of the tumor, which did not show any further progression on the final scan. He was readmitted for ascites, liver failure (SGOT 1,500, bilirubin 17), thrombocytopenia (platelet count 8,000), progressive hemiparesis, confusion, and somnolence. Despite treatment with Dilantin, Decadron, transfusions, vitamins, diuretics, and antacids he became progressively lethargic and intermittently agitated with the development of asterixis although the liver chemistries were improving. The platelet count dropped to 2,000 on 10/10/79. He was found unresponsive without a pulse or respirations the next night.
