[Spontaneous rupture of a splenic artery aneurysm during the third trimester of pregnancy]. / Rupture spontanée d'un anévrysme de l'artère splénique au cours du troisième trimestre de la grossesse.

We report the case of a 24-year-old female patient with spontaneous rupture of a splenic artery aneurysm in the third trimester of pregnancy. Pregnancy, throughout the physiological and hormonal changes it imposes, promotes the occurrence of aneurysm of the splenic artery and its rupture. Although this is a rare complication, its prognosis is severe and its typical clinical picture associating abdominal pain, hypotension and anemia is misleading for the clinician who likelier evokes a retroplacental hematoma or an uterine rupture. The maternal and foetal survival depends on rapid diagnosis and multidisciplinary management. Thus, it's important for the clinician to consider this differential diagnosis when abdominal pain or hemoperitoneum occurs in pregnant woman, particularly during the third trimester of pregnancy.

Nous rapportons l'histoire d'une patiente de 24 ans ayant présenté une rupture spontanée d'un anévrysme de l'artère splénique au cours du troisième trimestre de la grossesse. Celle-ci, de par les changements physiologiques et hormonaux qu'elle impose, favorise la survenue de l'anévrysme de l'artère splénique et sa rupture. Bien qu'il s'agisse d'une complication rare, son pronostic est redoutable et le tableau clinique typique associant douleur abdominale, hypotension et anémie est trompeur pour le clinicien qui évoque, plus volontiers, un hématome rétroplacentaire ou une rupture utérine. La survie materno-fœtale dépend de la rapidité diagnostique et d'une prise en charge multidisciplinaire, raisons pour lesquelles il est important que le clinicien considère ce diagnostic différentiel lors de la survenue d'une douleur abdominale ou d'un hémopéritoine chez la femme enceinte, particulièrement durant le 3ème trimestre de la grossesse.

Preeclampsia: an update.

Preeclampsia was formerly defined as a multisystemic disorder characterized by new onset of hypertension (i.e. systolic blood pressure (SBP) ≥ 140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 mmHg) and proteinuria (> 300 mg/24 h) arising after 20 weeks of gestation in a previously normotensive woman. Recently, the American College of Obstetricians and Gynecologists has stated that proteinuria is no longer required for the diagnosis of preeclampsia. This complication of pregnancy remains a leading cause of maternal morbidity and mortality. Clinical signs appear in the second half of pregnancy, but initial pathogenic mechanisms arise much earlier. The cytotrophoblast fails to remodel spiral arteries, leading to hypoperfusion and ischemia of the placenta. The fetal consequence is growth restriction. On the maternal side, the ischemic placenta releases factors that provoke a generalized maternal endothelial dysfunction. The endothelial dysfunction is in turn responsible for the symptoms and complications of preeclampsia. These include hypertension, proteinuria, renal impairment, thrombocytopenia, epigastric pain, liver dysfunction, hemolysis-elevated liver enzymes-low platelet count (HELLP) syndrome, visual disturbances, headache, and seizures. Despite a better understanding of preeclampsia pathophysiology and maternal hemodynamic alterations during preeclampsia, the only curative treatment remains placenta and fetus delivery. At the time of diagnosis, the initial objective is the assessment of disease severity. Severe hypertension (SBP ≥ 160 mm Hg and/or DBP ≥ 110 mmHg), thrombocytopenia < 100.000/µL, liver transaminases above twice the normal values, HELLP syndrome, renal failure, persistent epigastric or right upper quadrant pain, visual or neurologic symptoms, and acute pulmonary edema are all severity criteria. Medical treatment depends on the severity of preeclampsia, and relies on antihypertensive medications and magnesium sulfate. Medical treatment does not alter the course of the disease, but aims at preventing the occurrence of intracranial hemorrhages and seizures. The decision of terminating pregnancy and perform delivery is based on gestational age, maternal and fetal conditions, and severity of preeclampsia. Delivery is proposed for patients with preeclampsia without severe features after 37 weeks of gestation and in case of severe preeclampsia after 34 weeks of gestation. Between 24 and 34 weeks of gestation, conservative management of severe preeclampsia may be considered in selected patients. Antenatal corticosteroids should be administered to less than 34 gestation week preeclamptic women to promote fetal lung maturity. Termination of pregnancy should be discussed if severe preeclampsia occurs before 24 weeks of gestation. Maternal end organ dysfunction and non-reassuring tests of fetal well-being are indications for delivery at any gestational age. Neuraxial analgesia and anesthesia are, in the absence of thrombocytopenia, strongly considered as first line anesthetic techniques in preeclamptic patients. Airway edema and tracheal intubation-induced elevation in blood pressure are important issues of general anesthesia in those patients. The major adverse outcomes associated with preeclampsia are related to maternal central nervous system hemorrhage, hepatic rupture, and renal failure. Preeclampsia is also a risk factor for developing cardiovascular disease later in life, and therefore mandates long-term follow-up.

[Obstetrical epidural analgesia and postpartum backache]. / Analgésie péridurale obstétricale et lombalgie du post-partum: un lien de cause a effet?

Backache is a common problem in the general population. The prevalence of backpain is increased during pregnancy and after delivery. Early studies have suggested that labor epidural analgesia might be associated with an increased incidence of backache in the postpartum period. However, these initial studies were retrospective and their design included several methodological deficiencies. All the prospective studies published afterwards (prospective cohort studies and 3 randomized controlled trials) yield the same result: there is no relationship between labor epidural analgesia and long-term postpartum backpain. Pregnant women must be aware of this in order to make an informed and appropriate choice about labor epidural analgesia, the most effective technique for intrapartum pain relief.

[Post-dural puncture headache: treatment and prevention]. / Les céphalées post-ponction durale: traitement et prévention.

Post-dural puncture headache (PDPH) is a common iatrogenic and incapacitating complication. Dural puncture can be intentional (spinal block, myelography,...) or accidental (epidural block). Risk factors are well described and the obstetric patient is at high risk for PDPH. The treatment of PDPH is not standardised. Many options have been proposed, but only the epidural blood patch has apparent benefits. A few measures have been suggested to prevent PDPH after unintentional dural puncture, but none has been shown to work with certainty.

[Is a coagulation blood test compulsory before neuraxial blockade for labor analgesia?]. / Faut-il prescrire systématiquement un bilan d'hémostase avant la réalisation d'une péridurale analgésique pour le travail en obstétrique?

Neuraxial blockade such as epidural, spinal or combined spinal-epidural analgesia is considered to be the best technique for labour analgesia. Even if epidural hematoma is a very rare complication of neuraxial blockade, it may result in severe and definitive neurological injuries. This rare complication is usually associated with coagulation abnormalities. This is the reason why many physicians order routine coagulation screening tests before performing neuraxial blockade. This practice is questionable from the evidence-based medicine and the economic point of view. According to the guidelines published by several scientific societies, no routine coagulation screening tests are required in the absence of any history or clinical suspicion of coagulation impairment. The aim of the present article is to delineate the appropriate attitude in this context.

[Treatment of severe preeclampsia: until when and for what risks/benefits?]. / Traitement de la prééclampsie sévère: jusqu' où, et pour quels risques/bénéfices?

The four major hypertensive disorders related to pregnancy are preeclampsia, chronic hypertension, preeclampsia superimposed upon chronic hypertension, and gestational hypertension. The development of hypertension and proteinuria in pregnancy is usually due to preeclampsia, particularly in a primigravida. These findings typically become apparent in the latter part of the third trimester and progress until delivery, but some women develop symptoms in the latter half of the second trimester, or intrapartum, or the early postpartum period. Preeclampsia is characterized as mild or severe. Severe hypertension, coagulopathy, thrombocytopenia, liver function abnormalities, and fetal growth restriction are features of severe disease. Laboratory evaluation should assess haemoglobin/hematocrit and platelet count, renal and hepatic function, as well as assessment of fetal well-being and growth. Timing of delivery is based upon gestational age, maternal and fetal condition, and the severity of preeclampsia. Maternal end organ dysfunction and nonreassuring tests of fetal well-being are indications for delivery at any gestational age. Antihypertensive treatment aims at protecting the mother from severe hypertensive encephalopathy, but may jeopardize the fetus. We recommend antenatal corticosteroids (betamethasone) be given to women with preeclampsia at 26 to 34 weeks of gestation. Magnesium sulfate is more effective than phenytoin for prevention of eclamptic seizures.

Effects of nitrous oxide on spectral entropy of the EEG during surgery under balanced anaesthesia with sufentanil and sevoflurane.

BACKGROUND: Spectral entropy of the electroencephalogram (EEG) has been proposed to monitor anaesthetic depth. We investigated the effect of nitrous oxide on response (RE) and state entropy (SE) of the EEG during lumbar disc surgery under anaesthesia with sufentanil and sevoflurane. METHODS: In an open study, anaesthesia was induced with propofol and sufentanil, and maintained with 2% end-tidal sevoflurane concentration in air/oxygen (FiO2 = 0.4) in 25 patients. During surgery, nitrous oxide was randomly administered either at 0 or at 60% end-tidal concentration in 10 (control group) and 15 patients (nitrous oxide group), respectively. RE and SE were recorded at 2.5 min intervals for 10 min before randomization and for 25 min either continuously (control) or after achieving the target nitrous oxide concentration. RESULTS: Two patients who received nitrous oxide were excluded from statistical analysis because of protocol violation. Nitrous oxide provoked a significant decrease in RE and SE from 46.2 +/- 11.1 and 44.3 +/- 11.1 to a lowest value of 27.8 +/- 8.3 and 27.1 +/- 8.9, respectively. The decrease in entropy persisted during the 25 min recording period. CONCLUSIONS: Addition of nitrous oxide during balanced anaesthesia with sufentanil and sevoflurane provokes a decrease in response and state entropy of the EEG during lumbar disc surgery.

Predictive accuracy of continuous propofol infusions in neurosurgical patients: comparison of pharmacokinetic models.

The performance of 10 pharmacokinetic models in predicting blood propofol concentrations was evaluated in patients during neurosurgical anesthesia. Eight patients-ASA category I or II, aged 49 +/- 18-years, weighing 71 +/- 20 kg, and scheduled for routine neurosurgery-were anesthetized with propofol and sufentanil using Ohmeda pumps controlled with a personal computer. Sufentanil was administered as a bolus of 0.3 microgram.kg-1, 5 min before induction of anesthesia, and infused at a constant rate of 0.5 microgram.kg-1.h-1 throughout the study. At induction, propofol was administered as a bolus of 1.5 mg.kg-1 followed by a continuous infusion of 6 mg.kg-1.h-1. During surgery, the propofol infusion rate was deliberately increased by 2 mg.kg-1.h-1 every 15 min up to 12 mg.kg-1.h-1. Arterial blood samples were drawn at the end of each infusion step for measurement of propofol concentrations by high-performance liquid chromatography. Measured propofol concentrations were compared with theoretical concentrations derived from 10 published pharmacokinetic models designed in different clinical settings. Each model has been assessed by calculating the median of the performance error, the median of the absolute performance error, and their 10th and 90th percentiles. Models designed for certain categories, such as children, young, or elderly patients who received propofol as a bolus injection, showed a bad predictive accuracy. The models of Gepts et al. (Anesth Analg 1987; 66:1256-1263, Anaesthesia 1988; 43(suppl):8-13), Tackley et al. (Br J Anaesth 1989;62:46-53), and Cockshott (Postgrad Med J 1985;61:55), derived from healthy patients receiving continuous propofol infusions, provided the best agreement between expected and measured propofol concentrations; they showed bias and inaccuracy lower than 17%. In conclusion, the accurate prediction of blood propofol concentrations from different continuous infusion rates in ASA I or II patients requires the selection of appropriate pharmacokinetic models derived from similar categories of patients and using a similar technique of propofol administration. However, in clinical practice, the selection of a specific set among the appropriate models is balanced by the interindividual variability in blood propofol concentrations adjusted to clinical effects.

Effects of two calculated plasma sufentanil concentrations on the hemodynamic and bispectral index responses to Mayfield head holder application.

The effects of two calculated plasma sufentanil (SUF) concentrations on the hemodynamic and bispectral index (BIS) responses to Mayfield head holder (MH) application were studied in 20 patients scheduled for intracranial surgery. Premedication consisted of hydroxyzine, alprazolam, and atropine given orally 1 hour before surgery. Anesthesia was provided with propofol (PPF) and SUF using a target-controlled infusion device. Patients were randomly assigned to one of two groups according to calculated plasma concentrations: 3 microg/mL(-1) of PPF and 0.5 ng/mL(-1) of SUF in group I (GI) and 3 microg/mL(-1) of PPF and 1 ng/mL(-1) of SUF in group II (GII). The MH was fixed 33.0+/-6.6 minutes (mean +/- SD) after induction. Systolic (SAP), diastolic (DAP), and mean arterial pressure (MAP) as well as heart rate (HR) and BIS were recorded 1 minute before pinning (baseline) as well as 1 minute (P1), 2 minutes (P2), and 3 minutes (P3) after pinning. Multivariate repeat-measured analyses of variance were applied to the baseline-subtracted measurements of hemodynamic and BIS values. Groups were compared using the Student's t test, and P < .05 was considered to be statistically significant. Patients' characteristics, baseline hemodynamic values, and BIS values were similar in both groups. A significant overall time effect was observed for all variables, but no significant overall SUF effect was detected. Increases in SAP, MAP, DAP, and HR did not differ significantly between groups. The increase in hemodynamic variables did not exceed 20% of baseline value in either group. In contrast, at P1, the increase in BIS over the baseline value was significantly higher in GI (15.0+/-7.9) than in GII (6.7+/-6.5). In conclusion, MH application was associated with a significant, although not clinically relevant, increase in hemodynamic variables whatever the calculated plasma SUF concentration (0.5 or 1.0 ng/mL(-1)). In contrast, the increase in BIS observed at pinning was significantly higher in patients with the lowest calculated plasma SUF concentrations. This suggests that the BIS response to noxious stimulation is modulated by the analgesic regimen.

Effects of ephedrine on the onset time of neuromuscular block and intubating conditions after cisatracurium: preliminary results.

We studied the effects of intravenous ephedrine on the onset time and the intubating conditions 2 min after a bolus dose of cisatracurium (0.15 mg kg-1). Thirty patients anaesthetized with sufentanil and propofol were randomly divided in 2 groups to receive either ephedrine (70 micrograms.kg-1) or saline, 5 s before propofol. Cisatracurium was administered after loss of consciousness. Neuromuscular block was assessed at the adductor pollicis using accelography. Tracheal intubation was performed 2 min after cisatracurium injection and rated as excellent, good, poor or bad. At intubation, neuromuscular block (% height of control T1) was greater in patients receiving ephedrine (36.1 +/- 25.8% vs 57.9 +/- 25.1%) (mean +/- SD). The frequency of excellent intubating conditions was higher after ephedrine (86.6%) than after saline (40.0%). The onset time of cisatracurium was shorter after ephedrine (167 +/- 64.8 s vs 234.9 +/- 63.1 s). Thus, a low dose of ephedrine given before induction of anaesthesia improves the intubating conditions 2 min after 0.15 mg kg-1 cisatracurium and this effect likely relates to a quicker onset of neuromuscular block.

Effects of mild hypothermic cardiopulmonary bypass on EEG bispectral index.

We studied the effect of mild hypothermic cardiopulmonary bypass (30 degrees C) on the EEG Bispectral Index in 10 patients undergoing elective CABG. BIS was recorded at 11 event-related time points during the procedure. After a significant decrease at the induction of anaesthesia, BIS was not further modified during the procedure. BIS was neither affected by surgical stimulation nor by CPB and mild hypothermia. We conclude that we did not find any reason to preclude the use of BIS to assess the hypnotic effects of anaesthetics during normothermic or mild hypothermic CPB.

Effects of target-controlled anesthesia with propofol and sufentanil on the hemodynamic response to Mayfield head holder application.

The effects of target-controlled anesthesia with propofol and sufentanil on the hemodynamic response to Mayfield head holder (MH) application were evaluated in 18 ASA I and II patients undergoing scheduled intracranial surgery. Premedication consisted of hydroxyzine, alprazolam and atropine given orally 1 h before surgery. Anesthesia was provided with propofol and sufentanil using a target-controlled infusion device; constant calculated plasma concentrations of 4 micrograms ml-1 propofol and 0.5 ng ml-1 sufentanil were maintained throughout the study. Muscle relaxation was obtained with atracurium and ventilation was controlled with air/oxygen. The MH was fixed 45 +/- 12 min (mean +/- SD) after induction of anesthesia. Heart rate and systolic, diastolic, and mean non invasive arterial pressure were monitored and recorded 5 min before induction of anesthesia (control), 1 min before MH application (MH-1), at MH application, and 1 and 2 min after MH application. Systolic, diastolic, mean arterial pressure, and heart rate increased significantly during and after MH application when compared with MH-1 values, but remained constantly lower than control. Hemodynamic parameters measured 1 min before MH application were significantly lower than control. The results of the study indicate that target-controlled anesthesia maintained with constant calculated plasma concentrations of 4 micrograms ml-1 propofol and 0.5 ng ml-1 sufentanil prevents the increase in arterial pressure and heart rate beyond control values following MH application but may induce some degree of arterial hypotension in the absence of nociceptive stimulation.

Recovery from neuromuscular block after an intubation dose of cisatracurium and rocuronium in lumbar disc surgery.

BACKGROUND AND OBJECTIVE: Residual muscle paralysis remains a concern for anaesthesiologists. This study investigated the recovery from neuromuscular block (NMB) after an intubation dose of cisatracurium (C) or rocuronium (R) in 32 patients undergoing lumbar disc surgery. METHODS: Anaesthesia was induced with propofol and sufentanil, and maintained with sevoflurane in nitrous oxide/oxygen. Patients were randomised to receive twice the ED95 of either cisatracurium (GC) or rocuronium (GR) before tracheal intubation. After placement in prone position, neuromuscular transmission was monitored at the wrist by accelerometry. NMB was antagonised when the TOF ratio (TOFR) was < 0.75 at muscle closure. The time from muscle relaxant to muscle closure, and to TOFR of 0.25 and of 0.50 were recorded. Data were analysed using Student's t-tests, chi-squared tests and two-way mixed-designed ANOVA's. The prediction probability (Pk) of the times from muscle relaxant to muscle closure, and to TOFR of 0.25 for the necessity to antagonize NMB was calculated in both groups. P < 0.05 was considered statistically significant. RESULTS: NMB was antagonized in 8 (GC) and 6 (GR) patients, respectively. The time from muscle relaxant to muscle closure was shorter in patients whose NMB was antagonized. The Pk of this time was significant in GC (0.85) but not in GR (0.69). In GR contrarily to GC, the times to a TOFR of 0.25 and 0.50 were longer in patients whose NMB was antagonized. The Pk of the time to TOFR of 0.25 was significant in GR (0.95) but not in GC (0.64). CONCLUSIONS: A single dose of cisatracurium or rocuronium may be associated to some degree of NMB at the end of lumbar surgery, depending on the duration of surgery and on the duration of action of the muscle relaxant which is more variable for rocuronium than for cisatracurium.

[Pseudoxanthoma elasticum and obstetric epidural analgesia: report of a case]. / Analgésie épidurale obstétricale et pseudoxanthome élastique : à propos d'un cas.

Pseudoxanthoma elasticum is a rare inherited disorder of the elastic tissue characterised by multisystem manifestations. Skin, eyes, gastro-intestinal system and cardiovascular system are the major affected systems. We describe the anaesthetic management of a parturient affected by this disease.

[Circulatory and respiratory problems in preeclampsia]. / Manifestations hémodynamiques et respiratoires de la prééclampsie.

The hemodynamic and cardiovascular changes seen during PE vary according to the natural history of the disease, its severity and eventual therapeutic measures taken. In the early stages of pregnancy, patients who will eventually develop PE, present with a blood pressure which even though within normal limits, is higher than in other women. Similarly, their cardiac output is higher with a normal or decreased peripheral vascular resistance. As soon as the clinical signs of the disease appear, the hemodynamic picture usually shifts toward that of a high peripheral resistance with low cardiac output. Sometimes however, a clinically hyperkinetic circulation may be demonstrated. In PE patients, cardiac preload pressures are usually normal even though the circulatory volumes are lower by 600 to 800 ml when compared to those found in normal pregnancy. The cardiac function is however usually preserved during PE. PE induces an exaggerated capillary permeability. This results in the worsening of the airway edema which may render the intubation very difficult. The increased capillary permeability contributes, among other factors, to the heightened risk of acute pulmonary edema. It is not justified to administer an anti-hypertensive treatment to PE women presenting with only moderate hypertension. An anti-hypertensive treatment must only be initiated whenever the hypertension is severe (i.e. SBP> or =160 mmHg and/or DBP> or =110 mmHg) in order to reduce the risk of maternal complications. In the absence of objective comparative data assessing anti-hypertensive agents for the PE patient, the choice of therapy relies predominantly on the practitioners' own experience. Systematic circulatory volume expansion has not been proven to improve the maternal nor the neonatal prognosis. Such treatment is to be reserved solely for situations in which correcting a hypo-volemia is absolutely necessary. The treatment of acute pulmonary edema in a PE patient is symptomatic and includes the administration of vasodilating agents and of diuretics. A benefit in setting-up an invasive monitoring of the pulmonary artery occlusive pressure has not been demonstrated. The sonographic surveillance of the hemodynamic state can however be useful in these circumstances.

Side effects of the addition of clonidine 75 microg or sufentanil 5 microg to 0.2% ropivacaine for labour epidural analgesia.

BACKGROUND: Sufentanil 5 microg and clonidine 75 microg produce a similar reduction in minimum local anaesthetic concentration of ropivacaine. The aim of the present study was to compare the side effects of two equianalgesic solutions by combining 0.2% ropivacaine with either sufentanil 5 microg or clonidine 75 microg for labour epidural analgesia. METHODS: In a prospective double-blind study, 60 women at 5 cm cervical dilatation were randomly allocated to receive 0.2% ropivacaine with either sufentanil 5 microg or clonidine 75 microg to initiate labour analgesia. The analgesic efficacy and side effects of the two mixtures were compared. RESULTS: Onset, duration and quality of analgesia and subsequent ropivacaine consumption were similar in the two groups. Hypotension was significantly more frequent and severe with clonidine than with sufentanil (systolic blood pressure <100 mmHg: 17/26 vs. 6/24, P <0.05; systolic blood pressure <90 mmHg: 5/26 vs. 0/24, P <0.05) resulting in more frequent ephedrine administration (11/26 vs. 2/24, P <0.05) and larger fluid requirements (1696 +/- 583 mL vs. 1264 +/- 407 mL, P < 0.05). Conversely, pruritus was more frequent with sufentanil than with clonidine (6/26 vs. 1/24, P <0.05). CONCLUSIONS: Hypotension occurs more frequently when clonidine is added to epidural ropivacaine instead of an equianalgesic dose of sufentanil. Therefore, clonidine cannot be recommended for routine administration for labour epidural analgesia.

Management of severe preeclampsia.

Features of severe preeclampsia include severe proteinuric hypertension and symptoms of central nervous system dysfunction, hepatocellular injury, thrombocytopenia, oliguria, pulmonary oedema, cerebrovascular accident and severe intrauterine growth restriction. Women with severe preeclampsia must be hospitalized to confirm the diagnosis, to assess the severity of the disease, to monitor the progression of the disease and to try to stabilize the disease. Severe preeclampsia may be managed expectantly, in selected cases. The objective of expectant management in these patients is to improve neonatal outcome. Expectant management is based on antihypertensive treatment and prevention of end organ dysfunction. Antihypertensive treatment improves maternal outcome but has the potential to be deleterious for the foetus. Plasma volume expansion has been suggested for severe preeclampsia but trials failed to show any benefit. Magnesium sulfate is the anticonvulsivant of choice to treat or prevent eclampsia when indicated. Antenatal corticosteroids are recommended in severely preeclamptic women with 26-34 weeks gestation. Timing of delivery is based upon gestational age, severity of preeclampsia, maternal and foetal risks.