Acute airway obstruction following placement of a subclavian Hickman catheter

The purpose of this case report is to describe the events, intervention, and aetiology which led to acute airway obstruction in an adult patient after the placement of a Hickman catheter. Airway obstruction secondary to superior vena cava obstruction occurred after placement of a subclavian vein Hickman catheter. This was felt to occur, in part, to a narrowed superior vena cava as evident by subclavian venography. It resulted in emergency oral tracheal intubation to relieve airway obstruction. Shortly after removal of the Hickman catheter, the signs of superior vena cava obstruction syndrome resolved and the patient was extubated without incidence. It is concluded that, although rare, the serious complication of acute airway obstruction can occur after placement of a Hickman catheter.     

Adjuvant propofol enables better control of nausea and emesis secondary to chemotherapy for breast cancer

We investigated the prophylactic antiemetic effect of added lowdose infusion of propofol in patients exhibiting nausea and vomiting refractory to dexamethasone and serotonin antagonist during non-cisplatin chemotherapy for breast cancer. In a prospective open longitudinal study, 117 patients who had more than five episodes of nausea and vomiting in their first chemotherapy cycle during the first 24 hr completed the study. They received in addition to the usual prophylactic antiemetic regimen a continuous intravenous infusion of 1 mg · kg^?1 · hr^?1 propofol started four hours before chemotherapy and continued up to 24 hr for the two subsequent cycles. The number of vomiting / nausea episodes, level of sedation, patient activity, appetite and preference for future chemotherapy cycles were assessed. In the propofol supplemented cycles 90 and 80% of patients, during the 1st and 2nd propofol-assisted cycle respectively, were free of nausea and vomiting during the first 24 hr after chemotherapy. Patients were more frequently active and had more appetite during the propofol-assisted cycles. No propofol-associated side effects were observed. We conclude that the addition of a subhypnotic infusion of propofol enables better control of nausea and vomiting caused by non-cisplatin chemotherapy in the first 24 hr post-treatment.     

Epidural anaesthesia for elective Caesarean section does not influence fetal umbilical artery blood flow indices

This prospective study was completed to determine the influence of epidural anaesthesia on the fetoplacental circulation of normal subjects. Thirty-seven normal pregnant patients at term, undergoing elective Caesarean section, had Doppler measurements of the fetal umbilical artery blood flow velocity before and after epidural anaesthesia using lidocaine 2% without epinephrine. There were no differences in systolic/diastolic, resistance or pulsality indices following epidural anaesthesia. These results suggest that this technique has no adverse effect on fetoplacental circulation in normal non-labouring subjects. Cette étude prospective a pour but de déterminer l’influence de l’anesthésie épidurale sur la circulation foeto-placentaire dans le contexte d’une grossesse normale. Des indices de vélocité du flot de l’artère ombilicale foetale ont été mesurés par Doppler chez trentesept patientes gravides à terme, sans complications, programmées pour une césarienne élective, avant et après une anesthèsie épidurale utilisant la lidocaine 2% sans épinéphrine. Les indices de rapport systole/diastole, de résistance et de pulsatilité sont demeurés inchangés après l’induction de l’anesthésie épidurale. Ces constatations suggèrent que l’anesthésie épidurale n’a pas d’influence sur la circulation foetoplacentaire chez des patientes enceintes normales à terme qui ne sont pas en travail.     

Posterior approach to the lumbar plexus combined with a sciatic nerve block using lidocaine

A combination of lumbar plexus block, by a posterior technique, and sciatic nerve block can be a useful technique for outpatient anaesthesia. The purpose of this study was to examine the clinical characteristics of these blocks using lidocaine and to measure the serum lidocaine concentrations. Forty-five patients, undergoing lower extremity surgery, were studied. Sciatic nerve and lumbar plexus blocks were made with lidocaine, 680 mg with adrenaline 0.3 mg. For each patient the following data were collected: weight, age, sex, site of surgery, time to perform each block, needle depth, speed of onset of the sensory and motor blocks in the territories of the sciatic, femoral, obturator and lateral cutaneous (sensory) nerves and postoperative analgesic requirements. Lidocaine serum concentrations were measured in ten of these patients at 0, 2, 5, 10, 30, 60, 90 and 120 min after the second block. Analgesia was complete in 88% (40/45) of the patients. The remaining five patients needed analgesics (fentanyl 150 μg or less). Despite the high dose of lidocaine, the serum concentrations were within safe limits (mean ± SD) (C_MAX = 3.66 ± 2.21 μg · ml^?1). Only one patient had a serum concentration > 5 μg · ml^?1 (C_MAX = 9.54 μg · ml^?1). This was associated with a contra-lateral extension of the block. We conclude that this combination of blocks is a valuable alternative for unilateral lower extremity anaesthesia. However, clinicians must be aware of the implications of a contra-lateral extension of the block.     

Delayed awakening from general anaesthesia in a patient with Hunter syndrome

Hunter syndrome is one of a heterogeneous group of recessively inherited mucopolysaccharide storage diseases (MPS) with similar biochemical defects manifested by impairments in muco-polysaccharide catabolism with variable but progressive clinical courses. Abnormal accumulation and deposition of mucopoly-saccharides in the tissues of several organs lead to numerous anatomical, musculoskeletal and neurological abnormalities which are known to complicate anaesthetic and airway management. Hunter syndrome has a wide variance of clinical phenotypes ranging from mild to severe. We present a patient having physical and neurological features consistent with a severe clinical presentation of Hunter syndrome (MPS, Type II). Following a seemingly uneventful intraoperative anaesthetic course including isoflurane, nitrous oxide and fentanyl (0.93 μg · kg⁻¹), resumption of spontaneous ventilation and return to consciousness were delayed until intravenous naloxone (200 μg) was administered 100 min after the opioid administration. The cause of delayed recovery from anaesthesia in this patient is unknown. La maladie de Hunter fait partie du groupe des affections hétérogènes héréditaires et récessives des mucopolysaccharidoses (MPS) avec lesquelles elle partage les mêmes anomalies biochimiques. Celles-ci se manifestent par des altérations du catabolisme des mucopolysaccharides et une évolution variable et progressive. L’accumulation anormale de mucopolysaccharides dans les tissus de plusieurs organes provoque de nombreuses lésions musculo-squelettiques et neurologiques qui compliquent la gestion de l’anesthésie et des voies aériennes. Les phénotypes cliniques de la maladie de Hunter varient de légers à graves. Cette observation porte sur un patient qui présente des manifestations cliniques graves de la maladie de Hunter (MPS type II). A la suite d’une anesthésie sans problèmes réalisée avec de l’isoflurane, du protoxyde d’azote, et du fentanyl (0,93 μg · kg⁻¹), le retour normal à la ventilation spontanée et à la conscience est retardé jusqu’à l’administration de naloxone (200 mg) iv effectuée 110 min après le morphinique. La raison de ce retard est inconnue.     

Anaesthesia and the Sturge-Weber syndrome

We report a series of 13 patients with Sturge-Weber syndrome anaesthetised on 17 occasions. Anaesthesia management varied depending on the clinical manifestations which ranged from localized, superficial skin lesions to extensive systemic involvement. These patients tolerate anaesthesia well but anaesthetic management includes evaluation for associated anomalies. Difficulty with intubation may occur due to angiomas of the mouth and upper airway. Anaesthesia should be planned to avoid trauma to the haemangiomata and increases in intraocular and intracranial pressure. Nous rapportons une série d’observations concernant des porteurs du syndrome de Sturge-Weber anesthésiés à 17 occasions. L’anesthésie a varié selon les manifestations cliniques qui allaient de la lésion superficielle localisée à l’atteinte systémique grave. Ces patients tolèrent bien l’anesthésie mais celle-ci nécessite une recherche des anomalies associées pour fin d’évaluation. La présence d’angiomes de la bouche et des voies respiratoires supérieures peut rendre l’intubation difficile. La planification de l’anesthésie doit inclure la prévention du traumatisme aux hémangiomes et de l’augmentation de la tension intraoculaire et cérébrale.     

Vocal cord paralysis associated with difficult gastric tube insertion

Many clinical reports have described vocal cord paralysis after general anaesthesia. In most cases, paralysis was attributed to tracheal tube insertion. In this report we describe one patient in whom gastric tube insertion was strongly suspected as the cause of paralysis. The patient was a 47-yr-old man who underwent left hepatic lobectomy. Just after the operation he complained of hoarseness and a diagnosis of complete right vocal cord paralysis was made, from which he recovered after eight weeks. In this patient, insertion of the gastric tube seemed to have injured the anterior ramus of the right recurrent laryngeal nerve directly. Although there have been several reports of vocal cord paralysis induced by gastric tubes, none has noted such an acute onset and direct nerve injury. Therefore we would like to report this rare case and elucidate the mechanism of vocal cord paralysis. Careful attention should be paid in inserting a gastric tube to patients under general anaesthesia and, sometimes, the use of the soft tube may be indicated. Plusieurs publications portent sur la paralysie des cordes vocales après une anesthésie générale. Dans la plupart des cas, on attribue la paralysie à l’insertion du tube endotrachéal. Ce compte-rendu se rapporte à un cas où l’insertion d’une sonde gastrique est fortement mise en cause dans l’étiologie de la paralysie. Un patient de 47 ans subit une hépatectomie. Immédiatement après l’intervention, il se plaint de raucité de la voix et une paralysie de la corde vocale droite est diagnostiquée. La récupération s’effectue en huit semaines. Chez ce patient, la sonde gastrique semble avoir endommagé directement le rameau antérieur du nerf récurrent laryngé. Bien que plusieurs observations identiques de paralysie des cordes vocales provoquée par une sonde gastrique aient été publiées, aucune ne rapporte un début aussi soudain avec lésion nerveuse directe. Nous décrivons ici ce cas rare et tenterons d’expliquer le mécanisme de la paralyse de la corde vocale. Il faut être très prudent lorsqu’on insère un tube gastrique sous anesthésie générale et il est parfois préférable d’utiliser un tube mou.     

Intrathecal midazolam reduces isoflurane MAC and increases the apnoeic threshold in rats

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - The purpose of this study was to examine the anaesthetic requirement of intrathecal midazolam in a dose-response fashion in...     

Exacerbation of postdural puncture headache after epidural blood patch

The purpose of this report is to describe a new complication of epidural blood patch for inadvertent dural puncture. A dural tap in an obstetric patient was managed initially with a prophylactic blood patch via the epidural catheter. Despite this, 48 hr later, she developed post-dural puncture headache, neck, and shoulder pain, and was given a second epidural blood patch. This was followed by an immediate and severe exacerbation of her symptoms, which later resolved after the administration of diclofenac. There were no further sequelae. Although severe complications of epidural blood patch are rare, they are alarming. Exacerbation of the original symptoms of post-dural puncture headache caused by, or following, epidural blood patching has not previously been reported.     

Biotransformation of locally applied l-dopa in the corpus striatum of the hemi-Parkinsonian rat studied with microdialysis

Microdialysis was used to study the biotransformation of l-dopa in intact and denervated striata of rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of the substantia nigra. Microdialysis probes were placed in the intact and in the denervated striatum. Observations were then made on freely moving rats. Extracellular levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and 4-hydroxy-3-methoxyphenylacetic acid (homovanillic acid; HVA) were monitored before, during and after the local administration of l-dopa via the microdialysis probe for 20 min.A dose-dependent increase in extracellular dopamine levels was seen in intact striatum after application of l-dopa in concentrations ranging between 100 nmol/l and 10 mol/l. In the denervated striatum, the severity of the lesion influenced dopamine formation, so that no dose-effect relation could be established.The effects of the continuous intra striatal infusion of nomifensine, tetrodotoxin or benserazide on the l-dopa-induced dopamine outflow revealed that in the intact striatum this dopamine release is mainly voltage dependent. It was concluded that in the denervated striatum other cells of non-neuronal origin and containing aromatic l-amino acid decarboxylase make a major contribution to the increase in extracellular dopamine levels. Furthermore, l-dopa itself shows no dopamine-releasing properties, at least under the present experimental conditions. Correspondence to: S. Sarre at the above address