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Biomedical subjects

G Boulard

Publications and source records attributed to G Boulard.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1994

[Prehospital air ambulance and systemic secondary cerebral damage in severe craniocerebral injuries].

Advanced supportive therapy at the site of the accident, associated with direct transfer to a trauma centre increases survival and reduces morbidity rates. Patients with severe head injury, especially those with multiple injuries, often arrive in the emergency department with potentially causes of serious secondary systemic insults to the already injured brain, such as acute anemia (Hematocrit < or = 30%), hypotension (systolic arterial pressure (Pasys) < or = 95 mmHg, 12.7 kPa), hypercapnia (Paco2 > or = 45 mmHg, 6 kPa) and/or hypoxemia (Pao2 < or = 65 mmHg, 8.7 kPa). The incidence of such insults and their impact on mortality were studied in a group of 51 consecutive adults suffering from non penetrating severe head injury (Glasgow score < or = 8, mean age 31 +/- 17 yrs) rescued by a medicalized helicopter. Each patient received medical care on the site of the accident by an anaesthesiologist of a university hospital (UH) complying with an advanced trauma life support protocol including intubation, hyperventilation with FiO2 = 1, restoration of an adequate Pasys and direct transportation to the UH. Mean delay from call to arrival of the rescue team on the site was 15 +/- 5 min. Mean scene time was 32 +/- 10 min in cases not requiring extrication. Nineteen patients (Group I) were admitted without secondary systemic insults to the brain, 13 with isolated head injury, and 6 with multiple injuries, with a low Glasgow Outcome Score (GOS 1-3) of 42% at 3 months. In 32 patients (Group II), despite advanced supportive measures at the scene of the accident and during transportation, one or more secondary systemic insults to the brain were detected upon arrival at the emergency room, one with isolated head injury, 31 with multiple injuries, with a bad GOS of 72% at 3 months. We conclude that: 1) advanced trauma life support prevents from secondary systemic insults in the great majority of isolated severe head injured patients. 2) secondary systemic insults to the already injured brain are frequent in patients with multiple injuries and are difficult to avoid despite rapid aeromedical trauma care, 3) secondary systemic insults to the brain have a catastrophic impact on the outcome of severely head injured patients.

Adolescent↗
PubMed1994

[Treatment of hypovolemia in brain injured patients].

The appropriate administration of intravenous fluids in neurosurgical patients remains an area of disagreement between neurosurgeons and anaesthetists. Fluid restriction has long been advocated by the former and is widely believed to reduce or prevent the formation of cerebral oedema. However, such restriction can lead to hypovolaemia which in turn can result in haemodynamic instability. Thus, brain homeostasis should be aimed for through adequate fluid administration and normal or slightly elevated mean arterial pressure. The properties of the endothelium differ between the brain and the remainder of the body. In most non CNS tissues the size of the junctions between endothelial cells averages 65 A. Proteins do not cross these gaps while sodium does. In the brain, the junction size is only 7 A, which is too small to allow crossing by sodium. Investigations with changes in osmotic and oncotic pressure have demonstrated that: 1) reducing osmolality results in oedema formation in all tissues including normal brain; 2) a decrease in oncotic pressure is only associated with peripheral oedema but not in the brain; 3) in case of brain injury, a decrease in osmolality elicits oedema in the part of brain which remained normal; 4) similarly, a decrease in oncotic pressure does not cause an increase in brain oedema in the injured part of the brain. Thus, a major reduction in oncotic pressure is unimportant for the brain, whereas changes in total osmolality are the dominant driving force at this level. To conclude, in a hypovolaemic patient with severe head injury, the crystalloid of choice is NaCl 0.9% and the colloid of choice is hydroxyethylstarch, both with an osmolality > 300 mosm.kg-1. Ringer-lactate is hypoosmotic (255 mosm.kg-1) and may cause or increase cerebral oedema. Mean arterial pressure should be maintained above 80 mmHg.

Blood Pressure↗
PubMed1993

[Neuroanesthesia. Some new aspects].

Major changes are becoming apparent among neuro-anesthetists and neurosurgeons in their attitude towards hypocarbia, blood volume, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), anesthetic technique, and brain retraction pressure. These changes are related to the transfer from intensive care units to operating theaters of major new physiologic data regarding oxygen delivery to tissues (DO2) and oxygen consumption by tissues (VO2). These fundamental data have progressively, during the last five years, led to the concept of brain homeostasis based on four fundamental therapeutic principles: 1) The use of moderate hypocarbia (as opposed to deep hypocarbia which should stay exceptional). 2) The use of a normal mean arterial pressure (MAP) and thus cerebral perfusion pressure (CPP) by promoting a. normovolemia, b. a hematocrit around 30% and c. a light anesthesia technique allowing rapid recovery. 3) The use of appropriate crystalloids (NaCl 0.9% rather than Ringer-Lactate, and no DW5) taking into account measured osmolality. 4) The optimisation of brain relaxation by combining an appropriate anesthetic technique, mannitol, head up (and head straight) position, together with a lumbar drainage.

Anesthesia, General↗
PubMed1992

A new way to monitor external ventricular drainage.

External ventricular drainage is prone to mechanical complications and monitoring the system is not easy. It requires repeated checking of the drip or the level of the drained cerebrospinal fluid (CSF) in the bag. It was thus proposed that an efficient method by which to monitor the complete external ventricular drainage system would be by continuously weighing the drained CSF. Using weighing scales, a converter, and a recorder, the CSF weight was displayed as a function of time (i.e., flow, if the specific gravity of the CSF is 1, which is usually the case as an approximation). This system was used in 16 comatose patients (11 with subarachnoid hemorrhages and 5 with hydrocephaly during 204 recorded periods of 22.7 +/- 2.8 hours (mean +/- standard deviation). The mean flow was 0.17 +/- 0.05 ml/min. A cessation of CSF flow was seen graphically as a plateau. This occurred 18 times because of obstruction, which was relieved before clinical worsening by making minor adjustments in 15 patients and by reinsertion of a drain in 3 patients. Nociceptive stimuli like tracheal suctioning were also clearly visible on the graph (increased slope, i.e., increased CSF flow). This type of external ventricular drainage monitoring appears to be safe and reliable, giving indications before changes in medical condition. The observed flow, however, is not equal to its rate of secretion but rather to the difference between CSF secretion and reabsorption.

Adolescent↗
PubMed1991

[Passive immunotherapy in AIDS: transfusion of plasma rich in anti-p25 antibody (phase I trial)].

The present study is a therapeutic trial of phase I, based on the principle of passive immunotherapy in acquired immunodeficiency syndrome (AIDS). Eighteen patients with full blown AIDS (stage IV C2 of CDC) were subdivided into two groups: nine receiving every two weeks 300 ml of plasma collected from HIV-1 seropositive symptomless (stage II or III of CDC) individuals, and nine (control group) receiving 300 ml of seronegative plasma at the same rythm and for the same period. Each patient received seven transfusions. Clinical and biological results during the transfusional and post-transfusional periods are reported.

Acquired Immunodeficiency Syndrome↗