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Biomedical subjects

J P Mustaki

Publications and source records attributed to J P Mustaki.

7 recordsLinked to original sources

[Anesthesia for epilepsy surgery].

Epilepsy is rather common, affecting 0.5 to 2% of the population. Numerous patients, particularly those resistant to the antiepileptic therapy, can be surgically treated after a thorough evaluation. Surgery for epilepsy can be carried out either under general or local anaesthesia with sedation. This second approach is reserved for the extirpation of foci localised in motor, sensory or language areas. During the preoperative anaesthetic evaluation, two specific points have to be taken into account: the psychological aspect and the antiepileptic medication. During the procedure, an electrocorticography with or without stimulation may be indicated, particularly when a perioperative stimulation is scheduled. Low doses of volatile agents are chosen, and no curare and large doses of benzodiazepines and barbiturates. Awakening takes place on the operation table for a rapid and reliable neurological evaluation. During procedures performed under local anaesthesia, the anaesthetist must be ready at any time to intubate the patient in order to secure the airway.

Anesthesia↗

[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↗

[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↗

MAC-awake of isoflurane, enflurane and halothane evaluated by slow and fast alveolar washout.

End-tidal anaesthetic concentrations at first eye opening in response to a verbal command during recovery from anaesthesia (MAC-awake), were measured for isoflurane (n = 16), enflurane (n = 16) and halothane (n = 14). MAC-awake was measured during either slow or fast alveolar washout. Slow washout was obtained by decreasing anaesthetic concentrations in predetermined steps of 15 min, assuming equilibration between brain and alveolar partial pressures. Fast alveolar washout was obtained by discontinuation of the inhalation anaesthetic, which had been maintained at 1 MAC for at least 15 min. Mean MAC-awake obtained with slow alveolar washout was similar for isoflurane (0.25 (SD 0.03) MAC), and enflurane (0.27 (0.04) MAC) and significantly greater than values obtained by fast alveolar washout (isoflurane: 0.19 (0.03) MAC; enflurane: 0.20 (0.03) MAC). The MAC-awake of isoflurane and enflurane was significantly less than that of halothane, which was 0.59 (0.10) MAC as evaluated by the slow and 0.50 (0.05) MAC as evaluated by the fast alveolar washout method. Recovery time from anaesthesia with fast alveolar washout was 8.8 (4.0) min for halothane, which was not different from isoflurane (15 (2.5) min), but significantly shorter than for enflurane (22 (10) min), reflecting differences in the anaesthetic concentration gradient between MAC and MAC-awake values. These data do not support the hypothesis of a uniform ratio between MAC and MAC-awake values.

Adolescent↗