Quentin J. Durward

Treatment of Ischemic Deficits from Vasospasm with Intravascular Volume Expansion and Induced Arterial Hypertension

In 58 patients with progressive neurological deterioration from angiographically confirmed cerebral vasospasm after spontaneous subarachnoid hemorrhage, arterial hypertension was induced in an attempt to improve their deficits. The most effective regimen consisted of intravascular volume expansion, blockade of the vagal depressor response, and the administration of antidiuretics and vasopressor agents. With this protocol, arterial blood pressure could be sustained at high levels for prolonged periods. Neurological deterioration was reversed in 47 patients, transiently in 4; permanent improvement occurred in 43. Complications experienced during therapy included pulmonary edema, dilutional hyponatremia, aneurysmal rebleeding, coagulopathy, hemothorax, and myocardial infarction. Elevating systemic arterial pressure in states of cerebrovascular insufficiency resulting from vasospasm is safe if meticulous attention is paid to physiological, biochemical, and hematological parameters, with the exception that it may be hazardous in the presence of an untreated ruptured or intact aneurysm. Intravascular volume expansion and induced hypertension are effective in reversing ischemic deficits from vasospasm provided that treatment commences before cerebral infarction and that adequate pressures are maintained for a sufficient period. The production of a hypervolemic state by the use of colloid and crystalloid infusion accompanied by atropine blockade of the vagal depressor response and blunting of the diuresis with vasopressin enables arterial pressure to be elevated for longer than 1 week.

Myoepithelioma of the skull: a case report.

Background and importance Myoepithelioma of bone is a rare osseous tumor thought to be related to myoepithelial lesions found at other anatomic sites such as the salivary gland and skin. These tumors are composed of varying proportions of epithelial and myoepithelial cells and exhibit a spectrum of biologic behavior ranging from benign to malignant. We present the first reported case of myoepithelioma of the skull. Clinical presentation A 20-year-old white woman presented with a persistent right parieto-occipital skull nodule, relating its presence to a fall on the site 2 years previously. The nodule had become painful in the past 2 months. Her past medical history and workup were otherwise unremarkable. The initial biopsy was inconclusive for diagnosis. The lytic bone lesion was subsequently resected, and histopathological examination showed a proliferation of epithelioid cells in a myxochondroid background. Fluorescence in situ hybridization studies revealed a rearrangement of the EWSR1 locus. The morphologic and molecular findings were consistent with the diagnosis of myoepithelioma of bone. Conclusion Six months after surgery, the patient is doing well with no evidence of recurrence. This case illustrates the clinical presentation, histopathology, and molecular findings of a myoepithelioma of the skull with successful surgical treatment. Because myoepitheliomas with benign morphological appearance may rarely act aggressively, long-term clinical follow-up is warranted.

Management of fractures of the thoracolumbar and lumbar spite

Eleven cases of fracture or fracture/dislocation of the thoracolumbar or lumbar spine were studied to determine the effectiveness of three methods of management of the injuries. Ten of the patients had a neurological deficit as well as a spinal injury. All cases were studied by computed tomographic (CT) scanning of the injury site before and after treatment. CT scanning was found to be superior to linear tomography in determining the degree of canal compromise by bone at the injury site. Eight patients underwent operation, with the aims of achieving spinal stability in unstable injuries and of decompressing neural structures. These 8 patients had received Harrington distraction instrumentation (HDI) as an initial procedure. In those patients with fracture/dislocations from flexion-rotation injuries and canal compromise resulting from bony malalignment, reduction of the fracture/dislocation by HDI resulted in stabilization of the spine and increase of the open canal area at the injury site. However, in those patients with canal compromise resulting from bursting fractures with retropulsed bone fragments, HDI did not reduce in bone fragments. Removal of the anterior vertebral body and the bone fragments, however, did result in significant improvement of the canal dimensions. A poor correlation was found between the degree of canal compromise as measured by the CT scanner and the resulting neurological deficit. Reasons for this are presented. Six of the 10 neurologically compromised patients, including 2 patients with stable bursting injuries and retropulsed bone fragments treated conservatively, had improved one grade on Frankels classification by 3 months after injury. The rate and degree of recovery were not related to the degree of canal decompression achieved at operation.