Biomedical subjects
Publications and source records attributed to L Steiner.
A case of spontaneous intra-aneurysmal thrombosis, verified angiographically, is reported in a patient with subarachnoid hemorrhage and without surgical intervention. The frequency of such an occurence and the factors involved are reviewed and discussed.
Four-vessel angiography was repeated in 56 patients with confirmed subarachnoid hemorrhage in whom the initial investigation was negative. Only one aneurysm was demonstrated. The results suggested that, with good technique, careful observation, and a complete four-vessel cerebral angiography, a false negative rate of less than 2% can be achieved. It is suggested that to repeat pan-angiography is seldom justified unless further bleeding episodes occur.
Our experiment seems to confirm the hypothesis, implying an active CBF autoregulation as one of the interacting four survival mechanisms during an intracranial hemorrhage. While our present study has indicated that the autoregulation operates during the initial bleed, it is fully conceivable that the autoregulatory capacity may be exhausted after recurrent hemorrhages. Earlier experiments (Häggendal et al. [1970]) showed that autoregulation is easily abolished for prolonged periods after periods of intracranial hypertension. Further experiments are necessary to evaluate the capacity of the cerebral autoregulation to withstand repeated intracranial bleeds.
To eliminate the occurrence of artefacts produced by clips on the CT images, the use of titranium clips is suggested. Tests in vitro and in vivo indicate that clips manufactured from 0.2 mm thick 99.9 per cent titanium do not cause artefacts. They are resistant to corrosion, nontoxic, effective, easy to handle, relatively cheap, and are visible on plain X-ray films.
The effects of repeated subarachnoid hemorrhages have been investigated experimentally in dogs. The main objectives were to determine the tolerance to repeated hemorrhage and to study the changes occurring during the repeated bleeds, in intracranial pressure, EEG, ECG, systemic arterial pressure and respiration. The natural course of an intracranial hemorrhage was simulated by shunting blood from a femoral artery through a drop recorder into five different sites in the craniospinal system: the chiasmatic cistern, a lateral ventricle, the cisterna magna, the lumbar subarachnoid space and into the cerebral tissue of the left frontal lobe. The hemorrhage was allowed to continue until it stopped spontaneously. Each bleed resulted in a transient rise in intracranial pressure to the level of the arterial pressure, followed by a return to a steady state value. The time taken for the attainment of the steady state was increasingly prolonged. The final steady state pressure increased with each bleed. Ultimately, a stage was reached where the hemorrhage resulted in a sustained high pressure at the level of the arterial blood pressure, producing failure of vital functions and an irreversibly isoelectric electroencephalogram. The average number of bleeds necessary to produce this state in the case of hemorrhage into brain parenchyma was 3 (range 2-4), into the lateral ventricle, 4 range 3-5), and into the cisterna chiasmatica, 5 (range 2-7). After 5 hemorrhages into the cisterna magna and the spinal subarachnoid space, a local resistance at the bleeding site was built up which prevented further bleeding.
The mechanism limiting the tolerance to repeated subarachnoid hemorrhages was analysed experimentally. Blood introduced by an extracorporeal femorointrathecal shunt or by injection, into five different sites of the cranio-spinal system in living and dead dogs, produced a progressive increase in the steady state CSF pressure after each subsequent bleed. The pressure increase was quantitatively related to the amount of blood entering the system. A comparison of the respective effects of injections of whole blood and of erythrocytes indicated that the red blood cells were the component which induced an increase in the outflow resistance by clogging the pathways of the cerebrospinal fluid. The increase in outflow resistance with each bleed resulted in a stepwise rise in pressure to a level incompatible with survival. The lethal volume of bleed was specific for each site of hemorrhage: namely for brain parenchyma 8.1 ml, lateral ventricle 16.2 ml, cisterna chiasmatica 17.7 ml, cisterna magna 30 ml, and spinal subarachnoid space 55 ml. The assumption that death might be a random event was discarded, the failure of vital functions being considered to be the result of the high intracranial pressure. Mock bleeds using intrathecal infusions of saline suggested that spatial decompensation rather than cumulative ischemic effects caused death.
A technique is described for post-mortem examination of brain specimens employing computer tomography, for accurate comparison with in vivo scanning, including subsequent cutting of specimens in sections corresponding to tomographic layers measured. Potential application of this technique to diagnosis of mammary tumours is discussed.
A method to quantify the size of intracerebral hematoma by computer tomography was tested experimentally. The size of the lesion could be calculated with an error of +/- 3 to 9 per cent. By correlating the volume of the hematoma to the level consciousness in 62 patients, it was found that the volume which induced coma was rather specific, corresponding to about 6 to 7 per cent of the intracranial volume. This observation may lead to a reassessment of present therapeutic concepts.
Specimens from a number of patients locally irradiated in the thalamus for intractable pain with a multiple gamma beam technique have been examined. The geometry of well circumscribed necrotic lesions was ascertained. No correlation was seen between the dimensions of the lesions and the size of the field, 3 mm X 5 mm or 3 mm X 7 mm, within the clinically useful dose range, 16 to 25 krad.
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Spectrophotometric examinations were performed on cerebrospinal and subdural fluids in subacute (five patients) and chronic (20 patients) subdural haematomas, with special reference to the diagnostic aid of CSF spectrophotometry. Spectrophotometric xanthochromia of haemorrhagic origin was found in all CSFs examined, while definite visible xanthochromia was observed in only 28% and the CSF was judged as colourless in 52% of those cases. Characteristic bleeding patterns were found spectrophotometrically in all the 20 CSFs examined within 24 hours after lumbar puncture, haematoma patterns being detected in 90-95% of the cases. In many cases the electrophoretically separated protein fractions of CSF and subdural fluids were spectrophotometrically examined. In conclusion, CSF spectrophotometry is a simple, fast, and extremely sensitive method, which in our opinion should be used routinely in the diagnosis of suspected subdural haematomas, if lumbar puncture is not contraindicated.
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