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The effect of decompressive trepanation was compared to that of surgical resection of the traumatized tissue in the course of traumatic brain edema in standardized experimental brain trauma. Following a right parietal cold injury, the following parameters were monitored continuously in 12 cats: ventricular pressure, epidural pressure over both hemispheres, arterial and central venous pressure and heart rate. The EEG was evaluated continuously, using a computer (power spectra). After catheterization of the superior sagittal sinus, cerebral arteriovenous differences of glucose, lactate, O2 and CO2 were calculated. 6 animals were treated surgically when showing elevated intracranial pressure ICP and markedly altered EEG. In 3 animals, the right hemisphere was decompressed by extensive resection of bone and dura. In 3 further animals, the softened brain tissue of the cold lesion was resected and the skull defect closed. 6 untreated animals were used in controls. A decompression by skull hemiresection for ablation of the injured cortex abolished the high intracranial pressure, but only the latter method seemed to prevent further damage. This could be demonstrated by the EEG registration, and by the normalization of arteriovenous metabolite differences. Only animals treated with edema resection had a normal arousal reaction and survived the trauma. The results indicate, that only an ablation of the local injury will prevent further damage to the brain. After decompressive trepanation alone, the progression of tissue edema is not interrupted. As can be seen from the literature, the poor results obtained even from extensive decompressive operations in traumatic brain edema, indicate that the further development of edema is independent of the intracranial pressure, whereas the favorable results of resection of lobar contusions show an interruption of the spread of dysbolism.
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PMID:Comparison of the effects of surgical decompression and resection of local edema in the therapy of experimental brain trauma. Investigation of ICP, EEG and cerebral metabolism in cats. 47 64

Controlled hyperventilation has shown to be an effective method of treatment in patients with pronounced brain edema and high ICP caused by accidental or surgical damage. This treatment has to be started as early as possible after the injury to avoid secondary changes and spreading cerebral edema leading to the impact of the brain-stem and thus irreversible brain damage. If conducted consequently, controlled hyperventilation will diminish mortality rate and increase the rate of valuable recoveries in all sorts of brain injuries.
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PMID:Post-traumatic and postoperative treatment of severe brain injuries with controlled hyperventilation. 101 32

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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PMID:The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction. 159 96

A severe herpes simplex encephalitis with documented intra-cerebral lesions and brain edema was treated successfully with acyclovir and beta-interferon. The increase in intracranial pressure during the second week was well controlled by ICP monitoring. Life-threatening pressure peaks were avoided through the use of thiopental, osmodiuretics, TRIS, and lidocaine.
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PMID:Neurological outcome after a severe herpes simplex encephalitis treated with acyclovir and beta-interferon. Time course of intracranial pressure. 232 56

Earlier studies by our laboratories indicated that severe fluid percussion injury in cats results in the development of significant brain edema. In this study we measured the spatial distribution of edema developed after both central and lateral modes of impact with the objective of determining the degree to which the edema volume may contribute to ICP elevation and neurologic deterioration. All animals developed a marked increase in tissue water, particularly in the brainstem. In laterally injured cats, the increase in brainstem water equaled the edema produced supratentorially. Adding the increase of brainstem edema and the edema volume of the supratentorial compartment, we found an average water increase of 1.125 cc in survivors and 2.492 cc in nonsurvivors. This represents a significant volume increase when it is considered that the average PVI of the normal cat is approximately 0.9 cc (6). However, we observed that the PVI was reduced soon after injury and at a time when it has been reported that water content was near normal levels (7). Taking these studies in concert, we believe that the early reduction in PVI is most probably due to vascular swelling. The developing edema further contributes to reductions in PVI, thus setting the stage for elevated ICP and the tissue impaction observed in nonsurvivors.
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PMID:Comparative studies of edema produced by fluid percussion injury with lateral and central modes of injury in cats. 239 17

The continuous epidural registration of intracerebral pressure showed that the pronounced brain edema which develops during the 4th to 14th day of an intracerebral hemorrhage could lead to an increase in intracerebral pressure (ICP greater than 25 mmHg) requiring treatment. During the therapy extensive ICP crises (ICP greater than 35 mmHg), lasting for 1 to 3 days and only controllable through high doses of glycerol and sorbitol, developed. Glycerol (50 g orally) and sorbitol (50 g i.v.) lowered the pressure during this phase for approximately 3 h and 1.5 h respectively. These time intervals were in accordance with the changes in plasma osmolality through the administration of both substances. Due to its longer efficacy, glycerol provides an important supplement or alternative to sorbitol therapy, especially as the permitted maximum dosage would have to have been exceeded in a treatment consisting exclusively of sorbitol. The duration of the decrease in intracerebral pressure lasted longer during the remainder of the treatment in the case of both substances, being decisively dependent on the intracerebral pressure intensity. The relatively harmless epidural measurement of intracerebral pressure allowed an optimal control of the brain edema therapy as the dosage of the hyperosmolar substances could be given exactly in accordance with the intracerebral pressure intensity and subsequently varying efficacy.
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PMID:[Intracranial pressure-controlled treatment of brain edema with glycerin and sorbitol in intracerebral hemorrhage]. 356 10

Four cases of unilateral traumatic cerebral lesion with secondary third nerve palsy are reported. These four cases were observed over the course of one year and represent 5% of all unilateral traumatic cerebral lesion observed in our department during that period. The clinical situation presumptive of tentorial herniation included: partial (2 patients) or total (2 patients) secondary third nerve palsy, homolateral to the cerebral lesion; noncomatose state with initial Glasgow verbal score of 3 or greater; slight or no contralateral deficit. The anatomic lesions are unilateral and included 2 cases of temporal hematoma, one case of hemispheric swelling with acute subdural hematoma, and one case of general brain edema with temporal hematoma; In all 4 cases the clinical course was favorable with medical treatment alone. Based on the clinical information (non comatose state) and CT-scans (basal cisterns present or slight compressed in 3 of 4 cases), the authors believe that there was no tentorial herniation; third nerve palsy occurred without axial compression. The authors analysed several of the accepted criteria for severe head injuries (GCS, CT-scan, and ICP) and referred to the literature in order to determine optimal patient management in such reversible situations that posed a danger of tentorial herniation. Repeated clinical examination and CT-scan for visualization of basal cisterns appeared to be the best criteria for therapeutic decision.
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PMID:[Unilateral traumatic temporal lesions and secondary involvement of the 3d cranial nerve. Role of medical treatment]. 372 45

The present studies were performed to determine whether cerebral edema will develop as a consequence of arterial hypertension and/or craniectomy. Arterial hypertension was induced for 30 minutes by inflation of a balloon catheter situated in the descending aorta, and a parietal craniectomy was performed. The cerebral edema noticed was evaluated by macroscopic and microscopic observations, BBB permeability of HRP and Evans blue and water content. In addition, ICP was measured in the cisterna magna and ICPP by a catheter-tip transducer. In arterial hypertension or craniectomy alone, some small areas of Evans blue extravasation with increased water content were seen in the cortex, which corresponded to the occipito-parietal parts of the arterial boundary zones. In contrast, when arterial hypertension was combined with craniectomy, these lesions extended further into underlying white matter with increased water content. Forty-eight hours later, extensive brain edema with a shift of midline structures developed on the side of craniectomy which differed from that in arterial hypertension or craniectomy alone. It is suggested that some hydrostatic pressure gradients, particularly between blood vessel and surrounding extracellular space and among different areas within the brain parenchyma, may play an important role in the development of brain edema.
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PMID:Cerebral edema associated with craniectomy and arterial hypertension. 402 78

Haemophilus influenzae type b (HIb) is the most common cause of bacterial meningitis in children with a mortality rate ranging from 1.6% to 14%. Most patients have a 2-3 day history of symptoms prior to admission. A few have fulminating disease with rapid neurological deterioration. Review of 191 cases of HIb meningitis revealed a mortality rate of 2.1% but all who died had fulminating meningitis (FM). Four of six patients with FM died. FM patients had symptoms for less than 24 hours before rapid neurological deterioration with increased ICP, seizures, coma and/or respiratory arrest. Review of 10 FM cases revealed that on admission, 5 had hypotension, 3 had thrombocytopenia, and 8 had coma. Typical CSF changes were seen in only 7. All fatal cases died within 24 hours. Brain swelling and tonsillar herniation were found at autopsy. SDS-PAGE outer membrane protein subtyping did not show one "killer strain". Animal and autopsy data suggest that diminished CSF outflow and cerebral edema contribute to increased ICP. To improve survival of FM patients, initial treatment must (1) decrease ICP below levels impairing cerebral perfusion, (2) maintain adequate ventilation and blood pressure, and include (3) LP when stable, (4) antibiotics, and (5) close monitoring. Utilizing these principles, two FM patients survived without major sequelae.
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PMID:Fulminating haemophilus influenzae b meningitis. 670 99

Brain edema represents a disturbance of the volume equilibrium which, in the early stages of formation, must be compensated for by a reduction in other fluid and blood compartments. When this compensation is inadequate, tissue pressure and intracranial pressure increase, the magnitude of which depends on the compliance of the tissue. Tissue pressure gradients develop within the same hemisphere and between hemispheres, but these pressure gradients are transient and dissipate within a few hours after injury. The rate of dissipation is proportional to the product of hydraulic tissue resistance and compliance. These tissue pressure gradients are small in magnitude, less than 15 mm Hg; however, studies with an infusion model of edema in animals show that they are more than sufficient to propel fluid through the parenchyma by a process of bulk flow. The distention caused by the fluid increases the conductance and compliance of the tissue. This biomechanical response favors the dissipation of pressure gradients, and as a result hydrostatic gradients can be sustained only with a continued leakage of fluid from the site of injury. Without a continued extravasation of fluid, equilibration of the tissue pressure to the level of the ICP occurs rapidly. For this reason, the role of hydrostatic gradients in the resorption process may be limited. The development of an infusion model allows more rigid control and simulates the edematous process. Ultrastructural studies of the infusion model have shown that the tissue changes are similar to those reported for vasogenic edema, with the exception that in the infusion model the blood-brain barrier remains intact in the vicinity of the lesion and is not compromised by the mechanical distention of the ECS. The response of the cerebrovasculature to the infusion edema is in contrast to the usual reduction of flow seen after cryogenic injury. The CBF remains constant despite increased tissue water, as confirmed by gravimetric technique. The CO2 reactivity of the vessels in the area of edema is reduced, but the autoregulation to changes in perfusion pressure remains intact. When arterial pressure is raised beyond the limit of autoregulation, the pressure increase of CBF in the edematous area is less than the rise of CBF in normal tissue and suggests a "false autoregulation" caused by an increased tissue pressure. The differences in both the intracranial pressure and CBF response between these two models suggests that other factors must be operative. The cryogenic injury is indeed a traumatic injury to the brain and cannot be simply characterized by the increase in brain tissue water. In some animals a vasomotor paralysis disrupting the vascular compartmental volume and leading to a rapid rise in ICP with eventual reduction of CPP and CBF may explain these differences. Release of vasoactive substances into the ECS is an exciting hypothesis and is an area of investigation ideally suited to the infusion edema process where chemical composition of the fluid can be easily controlled.
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PMID:Biomechanics of brain edema and effects on local cerebral blood flow. 745 51


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