Characteristics and Limits of Tolerance in Repeated Subarachnoid Hemorrhage in Dogs

Abstract

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.

Changes in CSF pressures during experimental acute arterial subdural bleeding in pig

“…Brain homeostasis. Autoregulation of cerebral blood flow, increased oxygen extraction and the inherent tolerance of cerebral tissue to ischaemia in intracranial hypertension, together contribute to survival of brain tissue during the period of intracranial hypertension33, 62,67,68,85,86 3. Intact coagulation system.…”

Arterio-venous epidural shunting in epidural bleeding radiological and physiological characteristics. An experimental study in dogs

“…2. Brain homeostasis, integrating several mechanisms (autoregulation of the cerebral blood flow and increased cerebral oxygen extraction; ischemia tolerance of the brain tissue which facilitates brain survival during the period of intracranial hypertension 11,18,[17][18][19][20]. 3.…”

Epidural haematoma: Pathophysiological significance of extravasation and arteriovenous shunting

“…The clinical deterioration may be explained by progressive intracerebral expansion in both patients. The total volume of intracerebral contusions and epidural haematomas (which were classified as large) might together have exceeded the critical volume threshold for clinical deterioration to appear ~5~, 72,74 A fracture was found in 29 out of 35 patients. It was present in all patients with verified shunts, and only in half of those who had none.…”

“…This pattern is usually followed irrespective of the origin, anatomical site, or the size of the bleeding source 56. [71][72][73][74] Studies by other authors on experimentally-induced epidural bleeds in dogs have suggested that they behave in a similar way 20 Clinical data from patients with epidural bleeds appear, however, to contradict the experimental results 1 3, 5, 7--10, 14 15, 18, 21, 26, 29, 30, 31, ~5, ~8, 40, 4~, 44, 45, 58 60, 61, 63, 65, 76 Thus the classical "latent interval" is easier to explain if one assumes the bleed to be longlasting, starting at the moment of trauma, progressing continuously, and causing clinical symptoms at a later stage. The demonstration of extravasation of contrast medium from lacerated meningeal vessels many days after trauma has also been regarded as being in favour of long-lasting bleeding.…”