Unilateral mydriasis after induction of anaesthesia

Unilateral mydriasis is a disturbing finding during anaesthesia and may indicate serious neurological injury. In addition, the assessment of abnormal neurological findings is limited during general anaesthesia, and therefore requires special consideration. I report finding a dilated right pupil (7 mm, nonreactive to light) after bronchoscopic tracheal intubation and induction of general anaesthesia in a frail, 74-yr-old woman with cervical subluxations and spinal cord impingement. The possible aetology of the unilateral mydriasis includes the effects of anaesthetic agents, stellate ganglion block, impaired venous return from the head and neck, acute intracranial mass lesion or an haemorrhagic event, direct eye trauma, pre-existing medical or surgical conditions, and inadvertent direct deposition of alphaadrenergic or anticholinergic agents in the eye. Consideration of these factors, the autonomic innervation of the eye, and an intraoperative “wake-up” test allowed satisfactory neurological assessment in this patient and surgery to proceed. Unilateral mydriasis, while unusual, may be seen during general anaesthesia and requires thorough knowledge of autonomic nerve pathways and pharmacology of the eye for correct diagnosis. In this case, mydriasis was considered to result from phenyl-ephrine/lidocaine spray which was used to provide topical anaesthesia to the airway.     

Unilateral convulsion after induction of anaesthesia with propofol

We report a case in which a 42-yr-old man suffered a unilateral convulsion immediately after i.v. injection of propofol, and was discovered subsequently to have an old contralateral cerebral infarct. This complication and the current information on the relationship between propofol and abnormal neurological activity are discussed.      

Clonidine at induction reduces shivering after general anaesthesia

Purpose

Postanaesthetic shivering occurs in 5–65% of patients. In addition to causing discomfort. it is associated with deleterious consequences. Our objective was to investigate the effect of 150μg clonidine, at induction of anaesthesia, on penoperative core and peripheral temperature, incidence of postanaesthetic shivering and patients’ perception of cold.

Methods

Sixty ASA 1 or 2 patients scheduled for elective orthopaedic limb surgery were randomly allocated to group 1. who received 150μg clonidineiv, or group 2, who received a saline bolusiv. before induction. In all patients, anaesthesia was induced with fentanyl and propofol and maintained by spontaneous respiration (via a laiyngeal mask airway) of oxygen, nitrous oxide and enflurane. Core (nasopharyngeal) and peripheral (dorsal hand) temperatures were recorded at induction and 15-min intervals. Nurses, unaware of the treatment groups, recorded visible shivering in the recovery room. When cognitive function returned, patients were asked to grade their perception of cold on a 10 cm linear analogue scale, higher scores indicating heat discomfort.

Results

While core temperature decreased and peripheral temperature increased in both groups, there was no difference between the groups at any time. However, there was a lower incidence of shivering in the clonidine group (20%vs 66.7%,P < 0.001). Patients receiving clonidine felt warmer; thermal comfort score (median interquartile range) 5.9 (5.0–7.2)vs 5.0 (4.5–6.0),P < 0.05).

Conclusion

Clonidine 150 giv at induction of anaesthesia reduces the incidence of shivering and patients’ subjective perception of cold on emergence from general anaesthesia.     

The impact of fluid optimisation before induction of anaesthesia on hypotension after induction

Intra-operative hypotension is a known predictor of adverse events and poor outcomes following major surgery. Hypotension often occurs on induction of anaesthesia, typically attributed to hypovolaemia and the haemodynamic effects of anaesthetic agents. We assessed the efficacy of fluid optimisation for reducing the incidence of hypotension on induction of anaesthesia. This prospective trial enrolled 283 patients undergoing radical cystectomy and randomly allocated them to goal-directed fluid therapy (n = 142) or standard fluid therapy (n = 141). Goal-directed fluid therapy patients received fluid optimisation based on stroke volume response to passive leg raise before induction; those with positive passive leg raise received intravenous crystalloid fluid boluses until stroke volume was optimised. Baseline mean arterial pressure was measured on the morning of surgery and on arriving in the operating theatre. This post-hoc analysis defined haemodynamic instability as either a > 30% relative drop in mean arterial pressure compared with baseline or absolute mean arterial pressure < 55 mmHg, within 15 min of induction. Forty-two (30%) goal-directed fluid therapy patients underwent fluid optimisation after finding an intravascular fluid deficit via passive leg raise testing; 106 (75%) goal-directed fluid therapy and 112 (79%) standard fluid therapy patients met criteria for haemodynamic instability. There was no significant difference in the incidence of haemodynamic instability between the goal-directed fluid therapy and standard fluid therapy groups using absolute mean arterial pressure drop below 55 mmHg (p = 0.58) or using pre-surgical testing or pre-surgical mean arterial pressure values as baseline (p = 0.21, p = 0.89, respectively); however, the difference in the incidence of haemodynamic instability was significant using the operating theatre baseline mean arterial pressure (p = 0.004). We conclude that fluid optimisation before induction of general anaesthesia did not significantly impact haemodynamic instability.     

Effect of hypercapnia on arterial hypotension after induction of anaesthesia

We evaluated the effectiveness of intentional hypercapnia against hypotension after induction of anaesthesia with thiopental and isoflurane (TI) or propofol (P). For each group, 24 patients were anaesthetized with thiopental 4 mg kg(-1) (TI) or propofol 2 mg kg(-1) (P) for tracheal intubation and then lightly anaesthetized with isoflurane at 0.6% end-expiratory concentration (TI) or by 6 mg kg(-1) h(-1) infusion of propofol (P). In both anaesthesia groups, patients were randomly assigned to either normocapnia (end-tidal CO(2) = 35 mmHg) or hypercapnia (end-tidal CO(2) = 45 mmHg), which were achieved through adjusting the tidal volume. Systolic arterial pressure (SAP) 15 min after intubation was compared with the preanaesthetic baseline value. Under normocapnia, both TI and P induced a comparable, statistically significant suppression of SAP by approximately 20 mmHg from baseline. Hypercapnia prevented the decrease in SAP in TI but not in P. No patient in the TI-hypercapnia group experienced SAP below 100 mmHg, unlike those in the other groups. In conclusion, mild hypercapnia was effective in the prevention of hypotension in patients receiving thiopental followed by 0.6% end-expiratory isoflurane, but not in patients receiving 6 mg kg(-1) h(-1) propofol.     

Recovery after single-breath halothane induction of anaesthesia in daycase patients

A single-breath technique of inhalational induction of anaesthesia allows intravenous induction agents to be avoided. We have investigated recovery from anaesthesia in 40 daycase patients, using tests of psychomotor function. Patients anaesthetised with inhalational induction awaken earlier than those who receive thiopentone, but not significantly earlier. There were no significant differences in postoperative psychomotor function between patients who received thiopentone and those who had inhalational inductions. Single-breath halothane, nitrous-oxide, oxygen induction is an alternative to intravenous induction in cooperative adults, but does not confer significant benefits in terms of recovery.     

Intubating conditions using cisatracurium after induction of anaesthesia with thiopentone

We studied tracheal intubation conditions produced by the muscle relaxant, cisatracurium, following induction of anaesthesia with fentanyl (2 μgkg⁻¹) and thiopentone (6 mgkg⁻¹). Sixty patients were randomly assigned to receive cisatracurium in a single bolus dose of either 0.15 or 0.20 mgkg⁻¹. Tracheal intubation was commenced 120 s after injection of the relaxant. The mean (SD) time taken to achieve intubation was significantly shorter in the 0.20 mgkg⁻¹ group (137 (16) s) than the 0.15 mgkg⁻¹ group (149 (12) s; p < 0.05). The intubating conditions were better after the larger dose. Our results suggest that when anaesthesia is induced using thiopentone, a dose of 0.20 mgkg⁻¹ of cisatracurium is recommended to ensure satisfactory intubating conditions.     

Unexpected neurological deficits following recovery from anaesthesia

Two cases of neurological dysfunction are presented. Neurological deficits after recovery from anaesthesia are unusual in young women perioperatively. In the first case, a 39-yr-old woman presented at 36-wk gestation with antepartum haemorrhage and in labour. Pregnancy had been complicated by pre-eclampsia and she underwent emergency Caesarean section under general anaesthesia without complication. The trachea was extubated when she was awake but almost immediately she became hypertensive, obtunded and reintubation was required. Her pupils became fixed and dilated but the Computerised Axial Tomogram (CT) was normal. A coagulopathy was evident. She made a full neurological recovery within 24 hr. On the same day, a previously healthy 4l-yr-old woman who had undergone uneventful surgery for uterine prolapse 24 hr previously developed headache, nausea and over the next four hours signs of progressive brainstem ischaemia. The CT scan showed oedema of the mid- and hindbrain. Brainstem death was confirmed 12 hr later and the post-mortem revealed acute dissection of the vertebral artery secondary to cystic medial necrosis. Such dramatic neurological sequelae are rare but the importance of identifying “at risk” groups is underlined as is early recognition of neurological injury postoperatively.     

Unexpected double-primary aortoenteric fistula resulting in massive bleeding after induction of anesthesia

We report a case of a patient with a double-primary aortoenteric fistula with an abdominal aortic aneurysm. A 75-year-old man was taken to the operating room for the repair of an abdominal aortic aneurysm and a suspected aortoenteric fistula between the aorta and sigmoid colon. Sudden onset of massive bleeding through the nasogastric tube occurred after the induction of anesthesia. Surgical exploration confirmed an unexpected aortoduodenal fistula. Primary aortoenteric fistula is extremely rare and difficult to diagnose, and may cause fatal bleeding. The possibility of the presence of aortoenteric fistula, including multiple types, should be considered in the anesthetic management of abdominal aortic aneurysm.     

Recurrent respiratory depression after total intravenous anaesthesia with propofol and alfentanil

Since first commented upon by Lamarche in 1984, several cases of recurrent respiratory arrest after alfentanil infusions have been reported. In all these cases the alfentanil infusions have been used to supplement conventional anaesthetic techniques with nitrous oxide and/or inhalational agents and in most cases rather high total alfentanil doses have been administered. We have seen two cases of severe recurrent respiratory depression in healthy patients after relatively minor procedures performed under total intravenous anaesthesia with propofol–alfentanil infusions, air–oxygen ventilation and muscle relaxation, where the alfentanil doses administered were quite small. These cases are presented in detail and compared within a tabulated presentation with the earlier published cases of alfentanil-related recurrent respiratory depression.     

Acute hemodynamic collapse after induction of general anesthesia for emergent pulmonary embolectomy

Patients undergoing pulmonary embolectomy often experience hemodynamic deterioration during induction of general anesthesia (GA). Therefore, we studied the incidence and possible risk factors for hemodynamic deterioration during GA induction. Fifty-two consecutive patients undergoing emergent pulmonary embolectomy at our institution were included. Hemodynamic collapse after GA induction was defined as hypotension refractory to vasopressor, inotrope, or fluid administration, requiring cardiopulmonary resuscitation followed by urgent institution of cardiopulmonary bypass (CPB). Demographic variables, comorbidities, specific location of thromboemboli, preoperative inotropic support, and anesthetic drugs used for GA induction were evaluated as possible risk factors. After GA induction, hemodynamic collapse occurred in 19% of patients (n = 10). However, the occurrence of hemodynamic instability was not predicted by any of the evaluated risk factors. In addition, the incidence of in-hospital mortality did not differ between hemodynamically stable or unstable patients (10%; 4 of 42 versus 10%; 1 of 10 patients, respectively). In conclusion, hemodynamic deterioration after GA induction develops frequently during emergent pulmonary embolectomy. On the basis of our experience from this study and the unpredictable nature of hemodynamic deterioration, we suggest that patients undergoing pulmonary embolectomy should be prepared and draped before GA induction, and a cardiac surgical team should immediately be available for emergent institution of cardiopulmonary bypass.     

Sevoflurane anaesthesia in children after induction of anaesthesia with midazolam and thiopental does not cause epileptiform EEG

Background. Sevoflurane is a methyl ether anaesthetic commonlyused for induction and maintenance of general anaesthesia inchildren. Sevoflurane is a non-irritant and acts quickly soinduction is usually calm. However, inhalation induction withhigh concentrations of sevoflurane can cause convulsion-likemovements and seizure-like changes in the electroencephalogram(EEG). Little is known about the EEG during maintenance of anaesthesiawith sevoflurane, so we planned a prospective trial of sevofluranemaintenance after i.v. induction with benzodiazepine and barbiturate,which is another common induction technique in children. Methods. EEG recordings were made before premedication withmidazolam (0.1 mg kg^–1 i.v.), during induction ofanaesthesia with thiopental (5 mg kg^–1), and duringmaintenance with sevoflurane (2% end-tidal concentration inair/oxygen without nitrous oxide) in 30 generally healthy, 3-to 8-year-old children having adenoids removed. Noise-free EEGdata of good quality were successfully recorded from all 30children. Results. Two independent neurophysiologists did not detect epileptiformdischarges in any of the recordings. Conclusion. Premedication with midazolam, i.v. induction withthiopental and maintenance of anaesthesia with 2% sevofluranein air does not cause epileptiform EEG patterns in children. Br J Anaesth 2002; 89: 853–6