PubMed Health⌕ Search

Biomedical subjects

G Boulard

Publications and source records attributed to G Boulard.

At least 19 recordsLinked to original sources
PubMed1998

[The effect of position on intracranial pressure].

The question as to whether the head and trunk of neurosurgery patients should be elevated remains controversial. This question is particularly important when intracranial hypertension is present. Head up position may have beneficial effects on intracranial pressure (ICP) via changes in mean arterial pressure (MAP), airway pressure, central venous pressure and cerebro spinal fluid displacement. However, in some circumstances, head up position may decrease MAP which in turn will result in a paradoxical rise in ICP through autoregulation mechanisms. Therefore, the degree of head elevation has to be titrated by evaluating the most adequate cerebral perfusion pressure (CPP) for each patient by means of transcranial Doppler or measurement of jugular venous blood oxygen saturation. Head elevation above 30 degrees should be avoided in all cases. In most patients with intracranial hypertension, head and trunk elevation up to 30 degrees is useful in helping to decrease ICP, providing that a safe CPP of at least 70 mmHg or even 80 mmHg is maintained. Patients in poor haemodynamic conditions are best nursed flat. CPP is thus the most important factor in assessment and monitoring when considering head elevation in patients with increased ICP.

Humans↗
PubMed1997

[Cerebral hemodynamics and intracranial hypertension].

Various cerebral aggressions, either primary or secondary, can lead to the development of raised intracranial pressure. The presence of an elevated intracranial pressure often results in cerebral ischaemia/hypoxia and, eventually, neuronal death. In face of this cascade of events, several therapeutic approaches have been suggested. Two management concepts for patients with raised intracranial pressure have retained the most attention in recent years: the first suggests a therapeutic increase in cerebral perfusion pressure with the objectives to improve perilesional collateral perfusion and decreased cerebral blood volume, and consequently intracranial pressure in areas where autoregulation is preserved. The second concept supports the diminution in perilesional capillary pressure with the aim of decreasing vasogenic oedema. Although these two concepts are antagonistic and cannot be used simultaneously, they are probably complementary in the sequence of therapeutic events of patients experiencing severe head injury. This article reviews these therapeutic concepts and their clinical applications.

Anesthetics, Intravenous↗
PubMed1996

[Clinical presentation and prognosis of brain tumors].

The diagnosis of a cerebral tumor is received as dramatic by the patient or his family on account of the fonctional and symbolic idea of the brain and the perspectives of neurosurgical and psychological disabilities. Nowadays it is simplified because actual techniques of imagery are atraumatic and reliable. So the first signs are not to be undervaluated. Prognostic depends of identifiable factors. They lead the choice of therapy and help the medical doctor for the treatment follow-up and for answering to the patient's life questions.

Adult↗
PubMed1996

[Peroperative risks in cerebral aneurysm surgery].

The perioperative complications associated with cerebral aneurysm surgery require a specific anaesthetic management. Four major perioperative accidents are discussed in this review. The anaesthetic and surgical management in case of rebleeding subsequent to the re-rupture of the aneurysm is mainly prophylactic. It includes haemodynamic stability assurance, maintenance of mean arterial pressure (MAP) between 80-90 mmHg during stimulation of the patient such as endotracheal intubation, application of the skull-pin head-holder, incision, and craniotomy. The aneurysmal transmural pressure should be adequately maintained by avoiding an aggressive decrease of intracranial pressure. Once the skull is open, the brain must be kept slack in order to decrease pressure under the retractors and avoid the risks of stretching and tearing of the adjacent vessels. If, despite these precautions, the aneurysm ruptures again. MAP should be decreased to 60 mmHg and the brain rendered more slack, in order to allow direct clipping of the aneurysm, or temporary clipping of the adjacent vessels. The optimal agents in this situation are isoflurane (which decreases CMRO2), intravenous anaesthetic agents (inspite their negative inotropic effect, they may potentially protect the brain) and sodium nitroprusside. Vasospasm occurs usually between the 3rd and the 7th day after subarachnoid haemorrhage. It may be seen peroperatively. The optimal treatment, as well as prophylaxis, is moderate controlled hypertension (MAP > 100 mmHg), associated with hypervolaemia and haemodilution, the so-called triple H therapy, with strict control of the filling pressures. Other beneficial therapies are calcium antagonists (nimodipine and nicardipine), the removal of the blood accumulated around the brain and in the cisternae, and possibly local administration of papaverine. Abrupt MAP increases are controlled in order to maintain adequate aneurysmal transmural pressure. Beta-blockers, local anaesthetics administered locally or intravenously, a carefully titrated level of anaesthesia, a maintained volaemia play a protective role. Cerebral oedema is sometimes already present at the opening of the skull or may arise later, due to a high pressure under the retractors, to the surgical manipulations of the brain or to brain ischaemia subsequent to temporary clipping. Its treatment is aggressive, with intravenous agents, mannitol, deep hypocapnia and/or lumbar drainage. Prophylaxis, according to the "brain homeostasis concept", is the preferred method to avoid these four peroperative accidents. It includes normal blood volume, normoglycaemia, moderate hypocapnia, normotension, soft manipulation of the brain and optimal brain relaxation.

Anesthesia, General↗
PubMed1995

[Neuro-anesthetic contribution to the prevention of complications caused by mechanical cerebral retraction: concept of a chemical brain retractor].

During most intracranial procedures, the microscope is used to allow the surgeon to work on structures which are deeply located in the brain. Under these circumstances, brain retraction is required for adequate exposure. It was rapidly suspected and later confirmed that brain retraction causes secondary brain damage. This is due not only to direct effect of the retractor on the cortical surface, but also because a pressure is generated under the retractor, on the brain tissue, which compromises local cerebral blood flow and local cerebral perfusion pressure, thus causing cerebral ischaemia. The need for retraction is increased if the lesion is located deeply and/or if the brain is tensed; thus the risk to generate ischaemic conditions is enhanced. These secondary surgical lesions are promoted and worsened by associated systemic conditions such as hypotension, hypoxaemia, hypercapnia. As an attempt to respond to the problem generated by surgical retraction, the "chemical brain retractor" concept is proposed. By compulsively rendering the brain as relaxed and compliant as possible, the chemical brain retractor should allow the surgeon to operate on without the use of a surgical brain retractor and, if such a retractor is still needed, to reduce the pressure under it. These goals are achieved with an osmotic agent like mannitol to improve brain compliance, and intravenous anaesthetic agents, moderate hypocarbia and a normal or elevated blood pressure, to minimize cerebral blood volume. In conjunction with the chemical brain retractor, two other manoeuvres should be used to enhance cerebral compliance: CSF drainage and moderate head up position during the procedure.

Anesthesia, General↗
PubMed1995

[Controlled hypertension and cerebral protection].

Among the techniques of cerebral protection, the use of controlled arterial hypertension is based on the following arguments: 1) Cerebral ischaemia is the final common pathway of any insult to the brain, particularly through secondary lesions. Causes of secondary cerebral lesions include pressure under the brain retractors, temporary clipping, arterial hypotension, hypoxaemia, anaemia and hypercapnia. 2) In the brain, the critical lower value for cerebral blood flow is around 25 mL.100g-1.min-1, under which two types of ischaemic areas can be defined: the penlucida type where cerebral function is abolished, without permanent cerebral lesion and the penumbra type where cerebral tissue recovers only if flow is rapidly restored. In the latter case the duration of ischaemia is very important. 3) Cerebral blood flow is maintained stable within a large range of variations of mean arterial pressure through the autoregulation mechanisms, which is based on vasomotricity of the cerebral circulation, which implies major variations in cerebral blood volume. However, autoregulation needs several dozens of seconds to be achieved. Therefore, sudden variations in mean arterial pressure are associated with short lasting but major variations in cerebral blood volume. 4) In case of increased intracranial pressure, a decrease in cerebral perfusion pressure causes cerebral vasodilation through the autoregulation mechanism, with an increase in cerebral blood volume which will, in turn, increase intracranial pressure and thus decrease cerebral perfusion pressure, and so on. This is the vasodilatory cascade. The therapeutical increase in mean arterial pressure will correct this phenomenon and decrease intracranial pressure. This is called the vasoconstrictive cascade.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1995

[Concept of secondary cerebral injury of systemic origin].

The prevention and treatment of secondary insults to the brain of systemic origin in severely head injured patients remain of utmost importance. Head injury remains the leading cause of traumatic death, being responsible for 50-60% of fatalities. Head-injured patients not only suffer from the primary injury at the time of trauma, but also from the secondary, largely ischaemic, brain damage that occurs later. Some of these insults are of extracranial origin (or systemic), such as arterial hypotension, hypoxaemia, hypercarbia and anaemia. Their impact on mortality and morbidity is extremely high and requires greater efforts in improving the care of head-injured patients. Systemic insults occur either before the patient reaches hospital or during interfacility transfer or, in a surprisingly large number of cases, within hospital during emergency procedures, intrahospital transport or during their stay in intensive care units. Hypoxaemia, although quite easy to treat, is still common. This calls for better and earlier protection of the airway, more systematic administration of oxygen to trauma patients and wider use of pulse oximetry. Arterial hypotension has even more dramatic consequences in severe head injury. Recent studies indicate that short episodes of hypotension may induce severe brain ischaemia, that will be present even after complete systemic haemodynamic restoration. The treatment of hypotensive episodes should be immediate and aggressive. In some circumstances, restoration of an adequate cerebral perfusion pressure may not be obtained sufficiently rapidly with fluids alone and may require early use of vasopressors. Optimal haemodynamic resuscitation of the trauma patient with haemorrhagic hypotension and severe head injury remains a special challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Ischemia↗
PubMed1995

[Cerebral protection: contribution of intravenous anesthetic agents].

The administration of an intravenous anaesthetic agent before experimental cerebral ischaemia in animals improves the functional and histological outcome. Cerebral ischaemia may be global or focal, complete or incomplete. Intravenous anaesthetic agents reduce the cerebral metabolic demand for oxygen (CMRO2) and abolish electrophysiological activity. This reflects a discontinuation of the functional neuronal activity with maintenance of its basic metabolic activity. The oxygen spared by the decrease in consumption, while reducing the functional activity, might be used by the neurons to sustain longer periods of ischaemia. This protective effect is also observed after pretreatment with either lidocaine or volatile agents, but their potentially deleterious vasodilating effect must be considered. Ketamine has recently been shown to antagonize NMDA receptors. The protective effect of barbiturates was experimentally demonstrated more than 30 years ago. They are still used as a reference. They reduce CMRO2, optimise the ratio between oxygen consumption and oxygen delivery and thus reduce cerebral blood flow and cerebral blood volume, as a result of the decrease of the metabolic demand. This might explain why a protective effect is seen in case of global or focal hypoxia with increased intracranial pressure, while no protection is documented in case of global cerebral ischaemia, such as after cardiac arrest, where EEG is immediately flat and ICP low. However, at doses required to obtain a protective effect, barbiturates induce deleterious side effects such as severe arterial hypotension, which limits their use. Cerebrovascular and cardiac surgery or surgery of the carotids are characterised by potentially ischaemic episodes which can be predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Intravenous↗