Cerebral arteriovenous malformations in children

The treatment of cerebral arteriovenous malformations (AVM) or vascular anomalies are challenging neurosurgical procedures for an anaesthetist. Large AVMs are uncommon in children. Only 18% of AVMs become symptomatic before the age of 15 yr. This series reviews the experience at this institution during the period of 1982 to 1992. The symptoms at the time of presentation are varied and include haemorrhage (50%), seizures and hydrocephalus (36%) or congestive cardiac failure (18%). Symptoms of congestive heart failure predominate in the new-born whilst neurological symptoms, such as stroke, seizures or hydrocephalus occur more commonly in infants and older children. Approximately one third of AVMs in childhood present acutely. Radiological investigations, e.g., CT scan, MRI and cerebral angiography are essential to identify the precise location of the lesion. Therapeutic intervention in the acute presentation may involve craniotomy for evacuation of haematoma and treatment of increased intracranial pressure (ICP). Control of seizures and congestive heart failure may take priority and allow time to plan the elective procedures of embolization and surgical excision of the AVM. Operative intervention is hazardous and peroperative complications can be expected in more than 50% of patients. The morbidity and mortality associated with cerebral AVM are high, especially in infants who present in the neonatal period with congestive cardiac failure. The overall mortality in this series was 20%. Children presenting with intracranial arteriovenous malformations require a multidisciplinary approach. The successful management of anaesthesia either for embolization or surgical resection necessitates an understanding of the disciplines of paediatric and neuroanaesthesia. Special care and specific attention to detail may contribute to reduce the high morbidity and mortality encountered in these compromised children.     

A comparison of sevoflurane with halothane,enflurane, and isoflurane on bronchoconstriction caused by histamine

This study was conducted to assess the effect of sevoflurane on lung resistance and compliance, and its responsiveness to histamine. We studied eight dogs to compare the effect of sevoflurane, isoflurane, enflurane, and halothane on bronchoconstriction caused by histamine. Baseline values of pulmonary resistance (R_L) and dynamic pulmonary compliance (C_dyn) were measured prior to administration of histamine. Histamine (2, 4, and 8 μg · kg⁻¹) were administered iv, and the values of R_L and C_dyn at the time of peak effect were recorded. Under 1 or 2 MAC anaesthesia, sevoflurane as well as the other three anaesthetics had no bronchoactive effects. The four anaesthetics, including sevoflurane, demonstrated inhibitory effect on increases in R_L and decreases in C_dyn caused by histamine. At 1 MAC anaesthesia, % changes in R_L caused by 2, 4, or 8 μg · kg⁻¹ of histamine were 38 ± 11, 85 ± 21, or 132 ± 24% (mean ± SE) for halothane, and 65 ± 11, 132 ± 15, or 172 ± 19% for sevoflurane, respectively. Sevoflurane was less effective than halothane in preventing increases in R_L. In preventing decreases in C_dyn, sevoflurane was less effective than halothane only at 8 μg · kg⁻¹ of histamine under 1 and 2 MAC anaesthesia. There was no difference in attenuating effect on changes in R_L and C_dyn between sevoflurane and isoflurane or enflurane. We concluded that sevoflurane was less potent than halothane in attenuating changes in R_L and C_dyn in response to iv histamine. Cette étude a été réalisée dans le but d’évaluer les effets du sévoflurane sur la résistance et la compliance pulmonaires en réponse à l’histamine. Les effets du sévoflurane, de l’isoflurane, de l’enflurane et de l’halothane sur la bronchoconstriction induite par l’histamine sont comparés sur huit chiens. Avant l’administration d’histamine, on mesure les valeurs initiales de la résistance (R_L) et de la compliance dynamique (C_dyn) pulmonaires. L’histamine (2, 4, 8 μg · kg⁻¹) est administrée par la voie veineuse et les valeurs maximales de la R_L et de la C_dyn sont enregistrées. Les quatre anesthésiques, dont le sévoflurane inhibent l’augmentation de la R_L et la diminution de la C_dyn provoquées par l’histamine. A MAC 1 d’anesthésie, les pourcentages de changement de R_L produits par 2, 4, ou 8 μg · kg⁻¹ d’histamine sont respectivement de 38 ± 11, 85 ± 21, ou 132 ± 24% (moyenne + SD) pour l’halothane, et de 65 ± 11, 132 ± 15, ou 172 ± 19% pour le sévoflurane. Le sévoflurane est moins efficace que l’halothane pour prévenir les augmentations de R_L. Le sévoflurane est moins efficace pour prevenir la diminution de C_dyn mais seulement à 8 μg · kg⁻¹ d’histamine sous anesthésie à MAC 1 et 2. Le sévoflurane, l’halothane et l’isoflurane ne sont pas de différents pour amortir les changements de R_L et C_dyn. Nous concluons que le sévoflurane est moins puissant que l’halothane pour diminuer la réponse à l’histamine de la R_L et de la C_dyn.     

Anaesthetic management of an asthmatic child for appendicectomy

A 13-yr-old boy was scheduled for emergency appendicectomy because of abdominal pain. His preoperative medical history was complicated by a recent hospital admission for management of asthma. He had presented to hospital seven days earlier because of dyspnoea, tachypnoea and oxygen desaturation to 77% on room air. Following admission, he required intensive non-ventilatory management of his asthma, including intravenous salbutamol, methylprednisolone, and aminophylline, as well as use of an ipratroprium bromide inhaler and 100% oxygen by mask. He was discharged to the ward, and continued on prednisone (deltacortisone), beclomethasone inhaler, ipratroprium inhaler, and salbutamol inhaler. During his ICU stay, he complained of nonspecific abdominal pain, interpreted as gastro-oesophageal reflux. After four days, he was discharged to the ward. On his sixth hospital day, he began to experience right-sided lower abdominal pain and right shoulder pain. A surgeon was consulted, and the patient was found to have a very tender right lower quadrant with guarding and rebound pain. He was therefore scheduled for appendicectomy; antibiotic therapy with ampicillin, gentamicin, and metronidazole was initiated.     

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.