[Intracranial subdural hematoma after obstetric dural puncture]. / Hématome sous-dural intracrânien après brèche dure-mérienne en obstétrique.

The authors report a case of subdural haematoma (HSD), which occurred following epidural analgesia for labour, complicated by post dural puncture headache (PDPH). A 26-year-old woman displayed a typical PDPH following epidural anaesthesia. On the sixth day, she was given a blood patch (BP), which was partially efficacious. Because of worsening of the headache, of disappearance of the postural characteristics, and of vomiting without focal neurological signs on the 9th day, a CT-scan was done. The CT-scan showed a small hemispheric subdural haematoma. The recovery was complete with only medical treatment. HSD is a rare serious complication of dural puncture. When the characteristics of PDPH change, HSD should be evoked even without focal neurological signs. An early diagnosis and the small size of the haematoma may allow HSD to be treated medically and avoid surgical evacuation.

[Electroencephalographic effects of sevoflurane in pediatric anesthesia: a prospective study of 20 cases]. / Effets électroencéphalographiques du sévoflurane à l'induction chez le jeune enfant: étude prospective sur 20 cas.

OBJECTIVE: To study electroencephalographic (EEG) changes in children during induction of anaesthesia with 8% sevoflurane. PATIENTS: Twenty patients were consecutively included (ASA I-II; aged: 13-101 months). MATERIAL AND METHOD: Prospective study; approved by the Ethics Committee; written informed consent obtained from parents; anaesthesia induced with 8% sevoflurane in oxygen; no premedication was given; to collect the EEG data, non-invasive electodes were installed before induction; EEG was recorded continuously and stored on a computer for later analyses (descriptive analysis). RESULTS: Myoclonics movements were observed during induction of anaesthesia in two boys. Myoclonics movements stopped spontaneously without therapy. Epileptiform EEG activity (spikes and poly-spikes, burst suppression) was observed. In the 18 others cases, during sevoflurane induction, EEG changed rapidly with an increase in the range of beta activity (> 13 Hz) (n = 15) and in slow (< 8 Hz) and delta activity (< 4 Hz). In 14 patients, at time of laryngoscopy, the EEGs showed monophasic slow data activity (sharp high-voltage slow waves). Periods of EEG isoelectrical (burst suppression) were seen without spikes in four cases. CONCLUSION: At 2 MAC, epileptiform EEG activity has been observed during sevoflurane anaesthesia. In a short group of patients, this raises the question of avoiding sevoflurane in patients who have a history of epilepsy.

[Evaluation of transfusion strategies during craniosynostosis repairs]. / Evaluation de la stratégie transfusionnelle au cours des craniosténoses.

OBJECTIVE: To evaluate the changes in transfusion practices during craniosynostosis surgery in children, with consideration of the transfusion-associated risks. STUDY DESIGN: Retrospective study. PATIENTS: The study included 64 consecutive craniosynostosis repairs by the same neurosurgical and anaesthetic team, over a period of 17 years. METHODS: The children were allocated into two groups. In group I (1980-1991), blood loss was compensated precisely from scalp incision on. In group II (1992-1996), transfusion was only started when blood loss crossed a calculated limit considered as acceptable. The mean criterion of judgment was the quantity of transfused blood in comparison with the theoretical blood volume. Mean preoperative and postoperative haemoglobin concentrations, estimated blood losses, volume of replaced blood and number of transfused patients were compared between the two groups with a two tailed Student's t test. RESULTS: The rate of non transfused children increased from 6% before 1991 to 39% after 1992%; conservely the rate of postoperative transfusions increased from 3 to 39%. CONCLUSION: The risks of blood transfusion favoured the development of new of more restrictive transfusion practices, even in haemorrhagic surgery. To limit blood transfusion in craniosynostosis surgery, a harmonious cooperation between surgeons and anaesthetists is essential and blood replacement must be based on a definite determination of the acceptable blood losses.

Differences between cerebral and cerebellar autoregulation during progressive hypotension in rats.

Autoregulation in the brain is essential to the maintenance of perfusion and hence to the normal functioning of the organism in the face of various hemodynamic challenges. The existence of prodromal symptoms preceding fainting suggests that cerebellar autoregulation could be altered earlier than cerebral autoregulation during the development of hypotension. The purpose of this study was to compare cerebral and cerebellar autoregulatory responses to hypotension induced by two rates of hemorrhage 1.5 and 2.0 ml/min. Cortical blood flows were measured simultaneously using laser Doppler flowmetry in rats. With increasing rate of hemorrhage, the kinetics of autoregulation were maintained in the cerebrum, whereas it caused a progressive loss in the efficacy of autoregulation in the cerebellum.

Autoregulation of human inner ear blood flow during middle ear surgery with propofol or isoflurane anesthesia during controlled hypotension.

UNLABELLED: We used controlled hypotension to obtain a bloodless cavity during middle ear surgery under an optical microscope. No previous study has assessed the effect of controlled hypotension on inner ear blood flow (IEF) autoregulation in humans receiving propofol or isoflurane anesthesia. In the present study, the IEF autoregulation was determined using laser Doppler flowmetry in combination with transient evoked otoacoustic emissions (TEOAEs) during controlled hypotension with sodium nitroprusside in 20 patients randomly anesthetized with propofol or isoflurane. A coefficient of IEF autoregulation (Ga) was determined during controlled hypotension, with a Ga value ranging between 0 (no autoregulation) and 1 (perfect autoregulation). During controlled hypotension with propofol, IEF remained stable (1%+/-6%; P > 0.05) but decreased by 25%+/-8% with isoflurane (P < 0.05). The Ga was higher during propofol anesthesia (0.62+/-0.03) than during isoflurane anesthesia (0.22+/-0.03; P < 0.0001). Under propofol anesthesia, there were individual relationships between TEOAE amplitude and change in IEF in four patients. Such a correlation was not observed under isoflurane anesthesia. These results suggest that human IEF is autoregulated in response to decreased systemic pressure. Furthermore, isoflurane has a greater propensity to decrease cochlear autoregulation and function than propofol. IMPLICATIONS: The present study shows that inner ear blood flow is autoregulated under propofol, but not isoflurane, anesthesia during controlled hypotension in humans during middle ear surgery. Further studies are needed to explore the postoperative auditory functional consequences of the choice of the anesthetic drug used in middle ear surgery.

Effect of anesthesia on transient evoked otoacoustic emissions in humans: a comparison between propofol and isoflurane.

The influence of general anesthesia (GA) on auditory brainstem responses (ABRs) has been widely studied in humans whereas few studies have been devoted as yet to its effect on cochlear micromechanical properties. This study was aimed at evaluating: (1) the effect of GA on transient evoked otoacoustic emissions (TEOAEs) in humans (n=10), and (2) to compare the effects induced by two different anesthetic agents: propofol (n=5) and isoflurane (n=5). The TEOAEs were continuously monitored together with hemodynamic patterns describing various measures of blood pressure. (1) The GA induced a decrease in TEOAE amplitude and TEOAE amplitude was significantly correlated with the hemodynamic patterns. (2) Both anesthetic agents were responsible for a decrease in TEOAE during the first 20 min of recording. Under propofol, TEOAE amplitude increased after 20 min whereas under isoflurane TEOAEs continued to decrease. Under propofol, TEOAE amplitude was correlated with blood pressure changes in a highly significant manner, whereas under isoflurane TEOAE levels were completely independent of such hemodynamic patterns. These results infer that (1) the GA induced a decrease in TEOAE amplitude, and that (2) TEOAE changes induced by propofol could depend on the concomitant hemodynamic changes whereas isoflurane could be responsible for TEOAE changes depending on both, hemodynamic changes and its own pharmacological properties.

Effect of head-upright tilt on the dynamic of cerebral autoregulation.

The effect of head-upright tilting on the rate of cerebral autoregulation was studied in 12 healthy volunteers (nine men and three women; age range 20-36 years). The dynamics of cerebral autoregulation was determined from the rate of change in cerebral resistance (RoR) during a drop in arterial blood pressure induced by rapid deflation of a 3-min ischaemic thigh cuff and from the ratio of changes in cerebral blood flow and arterial blood pressure (CAI) during the recovery period after the drop in arterial blood pressure. The test was performed supine and with 40 degrees head-up tilt (40 degrees HUT). Middle cerebral artery mean blood flow velocity was measured by transcranial Doppler simultaneously with peripheral arterial blood pressure using Finapres. The thigh cuff deflation induced a larger drop in arterial pressure during 40 degrees HUT [median -28% (25 percentile -36, 75 percentile -19)] than in the supine position [-16% (-23, -15)] (P < 0.01) and in cerebral resistance [supine: -12% (-15, -6); 40 degrees HUT: -15% (-20, -12); P < 0.05]. There was no significant change in RoR [15% s-1 (12, 15)] and CAI [1.9 (1.5, 3.1)] measured supine and during 40 degrees HUT [RoR: 13% s-1 (12, 15); CAI: 1.3 (0.99, 1.9)]. During the drop in arterial pressure, the relationship between arterial blood pressure and systolic peak-to-peak interval exhibited an hysteresis loop, indicating a cardiopulmonary and/or baroreflex activation that was not observed with cerebral resistance. The rate of autoregulation is an intrinsic property of the cerebral vascular bed and is not affected by the vasodilator state in the range of arterial blood pressure changes induced by the tight cuff method.

Sympathetic nerve regulation of cochlear blood flow during increases in blood pressure in humans.

The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BPS) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an alpha adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (delta CBF) were plotted against BPS increases at each stage of the ANS inhibition. The BR diminished significantly after alpha blockade, after alpha and beta blockade, and after alpha and beta blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BPS increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BPS exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, delta CBF decrease and delta CBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BPS around 160 mmHg before ANS blockade. For BPS below 160 mmHg, correlations between delta CBF and BPS were significant before inhibition and after inhibition of ANS. For BPS below 160 mmHg, BPS and delta CBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BPS below 160 mmHg, CBF response to the BPS increase was the same before and after ANS blockade, i.e. ANS control did not predominate: even so, for BPS above 160 mmHg, the CBF response to BPS increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BPS below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena.

Effect of nitric oxide blockade on the lower limit of the cortical cerebral autoregulation in pentobarbital-anaesthetized rats.

The role of nitric oxide (NO) in cerebral autoregulation is controversial. The purpose of this study was to compare the effects on the lower limit of the cortical cerebral autoregulation of the inhibition of NO synthesis by N omega-nitro-L-arginine (L-NNA) infusion to saline and phenylephrine in pentobarbital-anaesthetized rats. Variations of the cortical cerebral blood flow (CBF), the cortical cerebrovascular resistances, the mean arterial pressure and the lower limit of cerebral autoregulation were compared in three groups: a group pretreated with L-NNA (n = 8), a group pretreated with saline (n = 8) and a group pretreated with phenylephrine (n = 5). The laser-Doppler flowmetry continuously measured CBF. Controlled haemorrhage was performed after the intravenous infusion of L-NNA, saline, or phenylephrine. The lower limit of cerebral autoregulation of each rat was computed by the least-squares method. The lower limit of cerebral autoregulation was significantly higher after L-NNA infusion (74 +/- 5 mm Hg) than after saline (43 +/- 3 mm Hg; p < 0.01) or phenylephrine infusions (52 +/- 5 mm Hg; p < 0.05). In conclusion, the role of NO on the cerebral autoregulation has been controversial; our results confirm the hypothesis that NO exerts a significant role in maintaining the lower limit of cerebral autoregulation in pentobarbital-anaesthetized rats.

Cerebral blood flow and resistances during hypotensive haemorrhage in the rabbit: transcranial Doppler and laser-Doppler flowmetry.

Transcranial Doppler (TCD) determined cerebral blood flow velocity and laser Doppler flowmetry (LDF) measured cortical perfusion were simultaneously assessed during hypotensive haemorrhage in 15 anaesthetized rabbits. Systolic (Fsys), diastolic (Fdia) and mean (Fmean) blood flow velocities were recorded into the intracranial internal carotid (ICA) and basilar artery (BA). Resistance (RI = Fsys-Fdia/Fsys) and pulsatility (PI = Fsys-Fdia/Fmean) indices were calculated. Step decreases of 10 mmHg of mean arterial pressure (MAP) from 80 to less than 30 mmHg provoked a fall of LDF signal below 50 mmHg. Blood velocities decreased into BA below 40 mmHg, and below 50 mmHg into ICA indicating regional differences in cerebral autoregulation. Cortical resistances (resLDF = MAP/LDF) fell below 60 mmHg whereas RI and PI increased when MAP decreased into BA below 40 mmHg and ICA below 50 mmHg. A weak correlation was found between Fmean and LDF (BA: r = 0.55, P < 0.01 and ICA = 0.46, P < 0.01). Both RI and PI were poorly correlated to resLDF into BA (RI-resLDF: r = -0.39, P < 0.01; PI-resLDF: r = -0.39, P < 0.01) and ICA (RI-resLDF: r = -0.18, ns; PI-resLDF: r = -0.22, ns). Pulse pressure (systolic-diastolic pressure) correlated with RI (ICA: r = -0.62, P < 0.001; BA: r = -0.61, P < 0.001) and PI (ICA: r = -0.61, P < 0.001; BA: r = -0.62, P < 0.001). In conclusion, during haemorrhagic shock, TCD correlates with LDF and indicates regional differences in autoregulatory settings. However, Doppler indices do not reflect the changes in cerebral resistances because they are influenced by the changes in pulsatile pressure.

[Effects of buflomedil and naftidrofuryl on the human cochlear microcirculation measured by laser-Doppler]. / Les effets du Buflomedil et du Naftidrofuryl sur la microcirculation cochléaire humaine mesurée par laser-Doppler.

The aim of this study was to assess the effects on cochlear blood flow measured by laser-Doppler of two vasoactive agents known for their supposed effectiveness in the presbyacousy treatment (buflomedil, naftidrofuryl), 16 patients undergoing acoustic neurinoma surgery were studied. Cochlear blood flow (CBF) was continuously recorded after the head of the probe was inserted into the internal ear through the round window. Systolic arterial pressure (SAP) and heart rate (HR) were continuously recorded via an arterial cannula. Hemodynamic variations due to buflomedil (400 mg in bolus) and to naftidrofuryl (200 mg in bolus) were compared with those of sodium nitroprusside (500 micrograms in bolus) in each case with anova. Buflomedil did not alter CBF (0%), SAP (+0.14 +/- 1.7%), HR (+3.4 +/- 3.4%). Naftidrofuryl provoked a significant decrease (P < 0.05) of CBF (-14.5 +/- 7.55%), SAP (-13.7 +/- 4%), and a significant increase (P < 0.05) of HR (+8.5 +/- 3.5%); there is a relationship between CBF and SAP (r = 0.88 P < 0.05). NPS provoked a significant decrease (P < 0.01) of CBF (-34.7 +/- 7.7%) SAP (-26.8 +/- 5.4%) and a significant increase (P < 0.01) of HR(+14.7 +/- 7.3%) in the same way of naftidrofuryl (P < 0.01). In conclusion, human cochlear microcirculation depends upon pharmacological hemodynamic variations such as animal models or middle ear microcirculation. If buflomedil did not alter it, naftidrofuryl provoked a reduction by a direct vasodilator effect inducing hypotension like sodium nitroprusside.

[Cerebral aspergillosis in immunocompromised patients]. / Aspergillose cérébrale chez l'immunodéprimé.

Three cases of central nervous system (CNS) aspergillosis in immunocompromised patients are reported. All three had neurological symptoms with normal cerebrospinal fluid (CSF). The CT scan showed poorly defined low density lesions which were not enhanced by contrast medium. They also had pulmonary signs and fever despite antibiotic treatment. Aspergillus fumigatus was isolated from bronchoalveolar lavage fluid. Antifungal therapy was started promptly, associating amphotericin B, itraconazole and flucytosine. Unfortunately, they died within 2 days to 2 weeks after admission in the intensive care unit. Postmortem examinations revealed disseminated aspergillosis with colonization of brain, lung, heart and kidney. The CT scan signs were quite different from those seen with the more usual bacterial ring lesions. In immunocompromised patients, the agents responsible for producing these findings are Aspergillus, Nocardia, Cryptococcus, Toxoplasma and Mycobacterium tuberculosis. Signs involving organs other than the CNS, and an examination of the CSF, should provide elements for establishing a differential diagnosis. Early antifungal treatment is the only chance of survival. Recrudescent fever and pulmonary signs occurring in neutropenic patients after antibacterial antibiotic treatment has been started are sufficient criteria for empirically starting amphotericin B administration unless clinical judgement dictates otherwise.