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The pathophysiology and outcome following severe head injury in 85 children are presented. The commonest initial CT diagnosis was of acute brain swelling. This swelling was associated with an increased white matter density on the CT scan which decreased to normal concomitant with recovery and increased ventricular size. CBF measurements in 6 of these patients revealed an increased blood flow despite a decreased CMRO2 and clinical coma. This CT pattern of diffuse swelling is believed to be due to acute cerebrovascular congestion and hyperemia and not to edema. Because of this, all children were treated with endotracheal intubation and controlled hyperventilation as part of the initial management. Mass lesions were uncommon, 20%. ICP was monitored in 40 children. The ICP rose above 20 Torr despite therapy in 80% of children with decerebrate or flaccid coma and in only 20% of children with spontaneous motor function. The ICP was at its highest between the second and fifth day. Aggressive therapy to control the ICP, with barbiturates if necessary, was successful in 80% of the patients. The overall results were useful recovery in 87.5% of the children, 3.5% were left vegetative or severely disabled and 9% died.
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PMID:Pathophysiology, treatment and outcome following severe head injury in children. 45 99

In five baboons and 11 cats cerebral ischaemia was produced either by inflating an epidural balloon and or by ligating major arteries supplying the brain. Fifteen of the animals developed intracranial hypertension after cerebral ischaemia. If ICP were high, but still significantly lower than MABP, elevation of MABP by noradrenaline infusions was accompanied by a proportional increase of ICP. However, the increase of ICP was lower than that of MABP so that CPP was raised. CBF measured by the 133Xenon clearance technique was significantly increased by arterial hypertension in eight cases. The proportional increase of CPP and CBF by elevation of arterial blood pressure was substantially greater, the lower ICP was immediately after ischaemia. There was no effect of MABP in cases in which ICP equalled MABP.
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PMID:Effect of systemic arterial blood pressure on cerebral blood flow in intracranial hypertension. 81 13

Arachidonic acid solution (2 to 15 mg/ml) was infused into the right forebrain white matter of anaesthetised cats over three hours to evaluate its contribution to the genesis and pathophysiology of vasogenic brain oedema. The 0.6 ml infusion increased local white matter water content by a mean of 11.3 ml/100 g tissue but did not increase cortical water content. Histological studies revealed local expansion and trabeculation of the white matter with aggregations of granulocytic neutrophils in the venules and perivenular brain. The adjacent cortical cytoarchitecture was normal. The white matter around the infusion site was stained lightly and over a variable area (15-20 mm2) by intravenously administered Evans Blue dye 2%. Regional cerebral blood flow (rCBF) adjacent to the frontal infusion did not change significantly during the period of infusion and remained similar to rCBF in the contralateral hemisphere. Following the arachidonic acid infusion regional CBF CO2 reactivity was normal and three was no asymmetry of either cortical somatosensory evoked potential (SEP) or motor evoked potential (MEP) waveforms. The increase in brain water content and changes in the ICP and ICP related biodynamics (pressure-volume index, lumped craniospinal compliance and CSF outflow resistance) were similar to those seen following infusion of 0.6 ml saline. These studies suggest that free intraparenchymal arachidonic acid, at concentrations exceeding those occurring in most neuropathological conditions, can increase the normal brain parenchymal capillary permeability but does not disrupt focal cerebrovascular and electrophysiological function. The clinical implications of these findings are discussed.
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PMID:The contribution of arachidonic acid to the aetiology and pathophysiology of focal brain oedema; studies using an infusion oedema model. 166 51

The ICP monitoring is currently used in the treatment of the head injured patients in order to avoid dangerous increases of the pressure and critical reduction of cerebral perfusion pressure (CPP). The cerebral blood flow is dependent on the CPP and is kept constant, under normal circumstances, by autoregulation. When autoregulation is impaired or overwhelmed oxygen delivery becomes uncoupled to the metabolic needs of cerebral tissue: in such a condition the rate of oxygen extraction changes and the artero-jugular difference for O2 (AVDO2) reflects this change. The AVDO2 can be used as an estimate of the CBF and can detect a situation of hyperemia (low AVDO2) or ischemia (high AVDO2). In 224 comatose head injured patients the ICP was measured using ventricular or subarachnoid catheters: the CPP was continuously assessed and the outcome was evaluated six months after the trauma. In 45 patients the AVDO2 was studied and the data were corrected for a PaCO2 of 40 mmHg and investigated. The severity of the ICP is decisive for the prognosis and, accordingly, the number of times the CPP is below 60 mmHg plays a major role in the outcome. The mortality rate was 21% for the patients without ICP greater than 20 mmHg and 54% for the patients with severe increases in ICP. The mean values of AVDO2 were low, ranging around 4.6 vol%; only 4 patients showed some temporary evidence of ischemia, as assessed by an AVDO2 greater than 8 vol%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arterio-jugular difference of oxygen and intracranial pressure in comatose, head injured patients. II. Clinical correlations]. 175 72

CBF and ICP were measured in cats following cerebral cold injury and mannitol infusion. Mannitol was found to reduce the intracranial hypertension caused by the injury. The restoration of CBF and ICP was of short duration and was followed by a reduction of CBF and elevation of ICP. A repeated restoration of CBF by a second dose of mannitol was followed by a more severe impairment of CBF. The prolonged beneficial effect of mannitol on CBF after brain injury has to be reassessed.
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PMID:Transient effect on mannitol on cerebral blood flow following brain injury. 212 73

Cerebral blood flow was assessed as initial slope index by 133-Xenon inhalation in 36 patients with brain tumours subjected to osmotic dehydration. The following solutions were employed: I. 20% mannitol, II. 40% sorbitol, III. 10% glycerol. Parameters affecting blood rheologic properties as Hct, plasma viscosity, red blood cell aggregation and fluidity were simultaneously studied. CBF which was reduced in the oedematous hemisphere with brain tumour increased during infusion and thereafter by mannitol or sorbitol, respectively. The blood flow response to glycerol was more delayed, less intense, but maintained longer. Hct and plasma viscosity were significantly reduced by all osmotic agents, while red blood cell fluidity fell and aggregation rose under mannitol. It is concluded that sorbitol (40%) is superior for emergency treatment with high ICP, whereas glycerol seems to be preferable to improve cerebral blood flow in oedematous brain.
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PMID:Cerebral blood flow and rheologic alterations by hyperosmolar therapy in patients with brain oedema. 212 75

Continuous measurement of CBV and CBF by means of laser-Doppler flowmetry was performed to analyze the temporal profile of cerebrovascular response to water accumulation in an infusion model of brain oedema. Using this method, the effect of mannitol on CBV was also examined to determine how mannitol improves the intracranial pressure-volume relationship. The results show that: (1) The presence of an oedema generator elicits a continuous reduction of CBV and a transient reduction of CBF. With cessation of this mechanical force of oedema production, CBV and CBF return to control levels. (2) Mannitol increases CBV and PVI. The improvement of PVI might be due to an increase in CBV as well as ICP reduction.
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PMID:Effect of mannitol on intracranial pressure-volume status and cerebral haemodynamics in brain oedema. 212 81

Secondary mediator compounds are postulated to have a role in vasogenic oedematogenesis. They may also cause focal brain dysfunction due to their neuronal, axonal and glial modulating properties. Using the feline model of infusion brain oedema the effects of right frontal intracerebral infusion (200 microliters/hr for 3 hrs) of saline, bradykinin (10(-4) to 10(-6) M), arachidonic acid (10(-2) to 10(-3) M), 20% protein and four human glioma cyst fluids were evaluated. Somatosensory evoked potentials (SSEP), motor evoked potentials (MEPs), rCBF and rCBF CO2 reactivity (Hydrogen clearance). ICP, craniospinal compliance, local brain tissue water content (microgravimety), brain histology and BBB function (Evans Blue 2%) were measured. Brain water content increased locally from 69% to 79%, ICP increased (by mean 14 mmHg) and compliance decreased (mean 70%) and there were the histological features of brain oedema with all infusates. BBB opening occurred with Bradykinin (+), arachidonic acid (++), 20% protein ( ) and glioma cyst fluid (4+). Polymorphic and macrophage infiltrates were seen with all infusions but rCBF and MEPs remained normal. SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid. This study suggests that certain compounds in brain oedema fluid could mediate local brain dysfunction.
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PMID:The contribution of secondary mediators to the etiology and pathophysiology of brain oedema: studies using a feline infusion oedema model. 212 86

Forty-eight patients with subarachnoid haemorrhage were studied with repeated rCBF and CMRO2 measurements. Cortical rCBF was measured using xenon-inhalation technique. CMRO2 was calculated as AVDO2 x CBF. When first studied the 29 conscious patients showed relative hyperaemia with CBF at 50 ml and reduced CMRO2 at 2.17 ml. In the following week CBF decreased to 41. CMRO2 remained reduced and constant. The 19 unconscious patients showed initially pronounced reduction in CMRO2 to 1.26, followed by gradual increase to 1.73 in 4-5 days. Simultaneously CBF increased from 18 ml to slightly above 30 ml. In the conscious patients the early reduction in CMRO2 and the concomitant luxury perfusion may be explained by global ischaemia because of very high ICP at the time of the haemorrhage. The reduced CBF in the unconscious group could be due to increased ICP, as ventricular drainage increased CBF to levels of relative hyperaemia as demonstrated in one case. As no decrease in CMRO2 was seen during the first 2 weeks, it is suggested that ischaemia at the time of aneurysm rupture is the most important single factor in reduction of global CMRO2.
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PMID:Cerebral blood flow and metabolism following subarachnoid haemorrhage: cerebral oxygen uptake and global blood flow during the acute period in patients with SAH. 227 Jul 45

CPP reflects perfusion problems related to increased ICP or inadequate MAP. CPP is a most helpful and practical management tool. The relationship of CBF and CPP depends on cerebral vascular resistance (flow equals pressure divided by resistance). At present, we do not have a practical method to measure vascular resistance or CBV. A close relationship between an increase in CBV and increase in ICP exists. However, the relationship between CBF and ICP is more complex. Whereas CBV is strongly dependent on vasodilation and venous return, CBF is influenced by CPP, vascular resistance, viscosity changes, and focally or diffusely increased ICP. For instance, in hypotensive shock one finds a low CBF with an elevated CBV (and ICP) from vasodilation related to hypercapnia, anoxia, or acidosis. Nevertheless, about two thirds of patients with increased ICP after head injury have increased CBF (hyperemia) and increased CBV. This frequent hyperemia is one rationale for the wide usage of hyperventilation to treat increased ICP. It must be recognized that a group of patients may have ischemia caused by excessive hyperventilation therapy for increased ICP. The PaCO2 must not be allowed to decrease to 20 mmHg or lower, but in some patients a PaCO2 level of 21 to 25 may be predisposing to ischemia. Strong consideration is thus given to monitoring CBF and cerebral oxygen metabolism (arteriovenous oxygen content difference [AVDO2], CMRO2) in states of coma and increased ICP. In such patients, continuous infusion of mannitol may result in improved CBF, and hyperventilation therapy can be less aggressive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nonsurgical management of increased intracranial pressure. 270 May 10


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