Shigehito Sato

Anaesthetic management of a neonate with prenatally diagnosed cervical tumour and upper airway obstruction

We report the anaesthetic management of a mother, and airway management of a neonate with a prenatal diagnosis of cervical cystic hygroma causing upper airway obstruction. The mortality of such neonates due to upper airway obstruction is reported to exceed 20% following deliveries. Elective Caesarean section was performed under general anaesthesia, and in utero tracheal intubation of the neonate was accomplished under uninterrupted maternal-fetal circulation. By utilizing isoflurane and ritodrine, the heart rate of the neonate remained between 120 to 150 bpm for four minutes following uterine incision. We believe that it is important that a multidisciplinary approach be initiated for planning of airway management of the neonate soon after the diagnosis is made. Laryngoscopy blades larger than normal for neonates, and a portable Doppler to monitor the viability of the neonate were found to be useful in the management of the neonate during in utero tracheal intubation. Although estimated blood loss was not increased, nor did uterine atony occur postoperatively despite the use of ritodrine during Caesarean section, the efficacy and safety of ritodrine to delay placental detachment have not been proved.RésuméNous décrivons la conduite adoptée chez une mère enceinte et son enfant souffrant d’une obstruction des voies respiratoires supérieures causée par un hygroma kystique cervical diagnostiqué in utero. Le taux de mortalité du nouveau-né présentant ce type d’obstruction dépasse 20% après l’accouchement. Une césarienne sous anesthésie générale a été réalisée et la trachée du nouveau-né intubée in utero sans interruption de la circulation foeto-maternelle. Sous isoflurane et ritodrine, la fréquence cardiaque foetale est demeurée entre 120 et 150 pendant quatre minutes après l’incision utérine. Nous croyons en l’importance d’une approche multidisciplinaire pour planifier le contrôle des voies aériennes néo-natales dès que le diagnostic est posé. Des lames de laryngoscope plus grandes que celles qu’on utilise normalement et un Doppler portable pour monitorer la viabilité du nouveau-né ont été utiles pendant l’intubation endotrachéale in utero. Bien que la perte sanguine n’ait pas été excessive, et qu’il n’y ait pas eu d’atonie utérine malgré l’utilisation de la ritodrine pendant la césarienne, on n’a pas fait la preuve de l’efficacité et de la sécurité de ce médicament pour retarder la séparation placentaire.

The comparison of epidural fentanyl, epidural lidocaine, and intravenous fentanyl in patients undergoing gastrectomy.

This study was conducted prospectively to compare the effect of epidural fentanyl (EP-F), epidural lidocaine (EP-L), and intravenous fentanyl (IV-F) on hemodynamic and hormonal responses to surgery and postoperative analgesic requirement in 30 patients undergoing gastrectomy during isoflurane anesthesia. An epidural catheter was placed via the T8-9 interspace. Group EP-F received fentanyl 2 micro gram/kg in 10 mL saline, and Group EP-L, 10 mL 1.5% lidocaine, epidurally; Group IV-F was given fentanyl, 2 micro gram/kg, IV. Fifty percent of the original dose was repeated every hour. Hemodynamic data and plasma hormonal levels were compared between those before and those at 1 h after skin incision. The total number of analgesic administrations within the first 48 h post-operatively were compared. Group EP-L developed more frequent episodes of hypotension. Group IV-F required higher isoflurane concentrations and the plasma epinephrine levels increased more than in Groups EP-F and EP-L. In Groups EP-L and IV-F, the plasma antidiuretic hormone (ADH) level increased more than in Group EP-F. In Groups EP-F and IV-F, the plasma cortisol and adrenocorticotropic hormone (ACTH) levels increased more than in Group EP-L. The use of postoperative analgesics was significantly less in Group EP-F. In conclusion, in Group EP-F, attenuated hormonal responses to surgery was accompanied with less hypotension and postoperative analgesic requirements were reduced. (Anesth Analg 1995;81:1169-74)

Pre-embarkment Prognostication for Acute Paraquat Poisoning

1 In order to assess which laboratory parameters could be related to the prognosis of patients with acute paraquat poisoning, we reviewed the medical records of 160 patients who had ingested paraquat in an attempt at suicide. 2 Serum creatinine and potassium concentrations, arterial blood bicarbonate and base excess levels, arterial blood pH, volume of paraquat ingested and the strength of the urinary paraquat qualitative test (sodium dithionate colour reaction) on admission in the surviving patients were significantly different from those of the patients who died within 48 h of ingestion. 3 The relationship of the quantity Eq1 defined as: Eq1 = ([K +] × [HCO- 3]) / ([Cre] × 0.088) (mEq l-1 ) against the interval of time after ingestion to admission (T) had a significant correlation with prognosis (P < 0.01). Patients with Eq1 > (1500 - 399 × LogT) had a 90% survival rate, Eq1: (930 - 399 × LogT) < Eq1 ≤ (1500 - 399 × LogT) 38% and Eq1 ≤ (930 - 399 × LogT) 3%, P < 0.01.

A case of acute pulmonary edema and bulbar paralysis after local epinephrine infiltration

An unusual case in which pulmonary edema and intracranial hemorrhage occurred during adenotonsillectomy is presented. The possible causes of this intracranial hemorrhage are discussed, especially in relationship to local epinephrine infiltration.

Anaesthetic induction time for tracheal intubation using sevoflurane or halothane in children

The current study was designed to determine the anaesthetic induction time required for tracheal intubation (TimeEI) with equipotent inspired concentrations of 5% sevoflurane and 2.5% halothane in oxygen. TimeEI that prevents 50% and 95% of patients from coughing and gross purposeful muscular movements after intubation was defined as TimeEI50 and TimeEI95, respectively. Thirty‐six patients aged 1–7 years were enrolled in the study. Anaesthesia was induced via mask and when TimeEI attained a predetermined value, intubation was performed using an uncuffed tube. Each TimeEI at which tracheal intubation was attempted was predetermined according to the up‐and‐down method. When intubation was accomplished without gross purposeful muscular movements, it was considered a smooth intubation. Determination with this method revealed that TimeEI50 and TimeEI95 for the sevoflurane/halothane groups were 147/214 s and 194/255 s, respectively. In conclusion, it is possible to determine TimeEI using an inspired sevoflurane concentration of 5% and halothane 2.5% in oxygen. The technique with 5% sevoflurane seems more practical for paediatric anaesthesia induction in busy clinical situations.

Milrinone Versus Glucagon: Comparative Hemodynamic Effects in Canine Propranolol Poisoning

Glucagon has been reported to be one of the most effective treatments for severe beta-blocker poisoning. Recently, amrinone was suggested as an alternative therapeutic choice for beta-blocker poisoning. Milrinone, a derivative of amrinone, acts independently of beta-adrenoceptors and increases cyclic AMP. Therefore milrinone may also be effective in the treatment of beta-blocker poisoning. In the present study, we compared the effect of glucagon and milrinone in treating severe beta-blocker poisoning. Following the administration of 10 mg/kg propranolol i.v. over 10 min, heart rate, cardiac output, mean arterial pressure, stroke volume, and end tidal CO2 were depressed, while central venous pressure, and pulmonary capillary wedge pressure increased significantly (p < 0.05). Following the administration of saline (Group S, N = 3), glucagon 20 micrograms/kg (Group G, N = 5), and milrinone 300 micrograms/kg (Group M, N = 5), hemodynamic parameters were observed for 30 min. In group M, mean arterial pressure, cardiac output and stroke volume recovered to their baseline values, while central venous pressure and pulmonary capillary wedge pressure decreased. Although there were no significant differences between groups G and M, the heart rate, central venous pressure and pulmonary capillary wedge pressure, mean arterial pressure and stroke volume did not return to baseline values in group G. Milrinone administration produced a significant hemodynamic improvement without increasing the heart rate in the canine model of severe heart failure caused by propranolol. In the glucagon treatment group, central venous pressure and pulmonary capillary wedge pressure improved less than the milrinone group. Although more data are needed before a clinical recommendation, milrinone might be an effective drug to treat beta-blocker poisoning.

Elevated amylase is related to the development of respiratory failure in organophosphate poisoning

1 A retrospective study of organophosphate(OP) poison ing in the intensive care unit was performed to analyze the incidence of respiratory failure. 2 The patients were treated initially with gastrointest inal decontamination including gastric lavage and the administration of activated charcoal with cathartic. Further management included intravenous pralidoxim and atropine and ventilatory support. 3 Of the 32 OP poisoning patients, 16 patients developed respiratory failure and received ventilatory support. 4 An increase in plasma amylase above the normal range on the day of admission was related to the development of respiratory failure. 5 In OP poisoning, the elevation of amylase level was predictive of the subsequent respiratory failure.

Combined Use of Glucagon and Milrinone May Not Be Preferable for Severe Propranolol Poisoning in the Canine Model

In a previous study of propranolol poisoning, glucagon and milrinone significantly increased cardiac output, but the improvement caused by glucagon was almost entirely due to the chronotropic effect. This study investigates the combined effect of glucagon, in a dose not inducing tachycardia, and milrinone on beta-blocker poisoning. Following the administration of 10 mg/kg propranolol IV over ten minutes, dogs (N = 20) were divided into four treatment groups, group S (saline), group G (glucagon 2.5 micrograms/kg), group M (milrinone 100 micrograms/kg), and group G + M (glucagon 2.5 micrograms/kg plus milrinone 100 micrograms/kg). Hemodynamic parameters were observed over the next thirty minutes. Heart rate, cardiac output, and mean arterial pressure were decreased in all groups after the administration of propranolol. Heart rate, mean arterial pressure, cardiac output, and stroke volume recovered to the baseline values in group G + M. However, heart rate in group G + M showed a significant increase versus the other three groups. In a canine model of severe propranolol poisoning, the combined effect of glucagon 2.5 micrograms/kg and milrinone 100 micrograms/kg brought about a significant hemodynamic improvement, but it was accompanied by an excessive increase of heart rate. Combined therapy of milrinone and glucagon may not be preferable therapy in beta-blocker poisoning in the canine model.

Heart rate response to atropine in humans anaesthetized with five different techniques

Atropine, 0.01 mg·kg-1, was given intravenously before the start of surgery to 169 patients who were anaesthetized with one of five different techniques; halothane, enfturane, cervical epidural, lumbar epidural or narcotic anaesthesia in addition to nitrous oxide and oxygen. Atropine produced a significant increase in heart rate (HR) within 1 min in all patients studied; the HR increases in patients anaesthetized with halothane (37 ± 11 beats·min-1, n = 37) or narcotic (34 ± 12 beats·min-1, n = 30) were significantly greater than in those anaesthetized with enflurane (25 ± 10 beats·min-1, n = 35; P < 0.01) or epidural anaesthesia. Because of the presence of an acute cardiac sympathectomy, the patients who received cervical epidural anaesthesia were expected to have different responses to the atropine. However, there was no significant difference in the HR increases between the patient groups with cervical (19 ± 12 beats·min-1, n = 32) and lumbar (22 ± 8 beats·min-1, n = 35) epidural anaesthesia. Atropine also produced a small but significant increase in arterial pressure in all five groups of patients. These results suggest that the cardiac responses to atropine may differ depending on the individual anaesthetic agent used, and are likely dependent upon the agent’ s effect on autonomic nervous system activity.RésuméDe ľatropine 0.01 mg · kg-1 a été administré par voie intraveineuse avant le début de la chirurgie à 169 patients qui étaient anesthésiés avec ľune des cinq techniques différentes; halothane, enflurane, épidurale cervicale, épidurale lombaire ou anesthésie au narcotique additonné de protoxyde ďazote et ďoxygène. Ľatropine a produit une augmentation significative de la fréquence cardiaque (HR) en dedans ďune minute chez tous les patients étudiés. Cette augmentation de la fréquence cardiaque chez les patients anesthésiés avec ľhalothane (37 ± 11 BPM, n = 37) et narcotic (34 ± 12 BPM, n = 30) étaient significativement plus grandes que celles observées avec ľenflurane (25 ± 10 BPM, n = 35; p < 0.01) et ľanesthésie épidurale. A cause ďune sympathectomie cardiaque aiguë les patients ayant reçu une anesthésie épidurale cervicale on anticipa une réponse différente lors de ľadministration de ľatropine. Cependant on observa aucune différence statistiquement significative dans ľaugmentation de la fréquence cardiaque entre ľanesthésie épidurale cervicale (19 ± 12 BPM, n = 32) et lombaire (22 ± 8 BPM, n = 35). Ľatropine a aussi produit une petite augmentation statistiquement significative dans la pression artérielle chez les patients des cinq groupes. Ces résultats suggèrent que la réponse cardiaque à ľatropine peut varier selon ľagent anesthésique utilisé selon ľeffet de ľagent sur ľactivité du système nerveux autonome.

Arteriovenous differences in PCO2 and cardiac output during CPR in the dog

Using 14 mongrel dogs, we investigated the correlation between arteriovenous differences of PCO2 (AVD-CO2) and cardiac output (CO) during CPR. Ventricular fibrillation was induced by an electrical current and the respirator was stopped for 5 min. Cardiopulmonary resuscitation (CPR) was performed during the next 10 min and CO was measured with simultaneous arterial and venous blood gas analysis. CO was measured 26 times during CPR. The animals were divided into two groups according to the values of CO during CPR: low-CO group (CO < 0.3 l/min) and high-CO group (CO > or = 0.3 l/min). AVD-CO2 in the low CO group was 39.8 +/- 5.7 mmHg and that of the high group was 27.4 +/- 14.8 mmHg (mean +/- S.D., P < 0.05). In conclusion, AVD-CO2 showed an inverse result with the degree of CO during CPR.