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Purpose: Lumbar subarachnoid catheters for cerebrospinal fluid (CSF) drainage (lumbar drains) are indicated for several medical and surgical conditions. A number of complications can occur from the placement of this type of catheter, including catheter breakage from excessive traction or shearing over the Tuohy needle., Clinical Features: Five cases of lumbar subarachnoid catheter breakage/shearing and catheter fragment retention, as well as one near miss, were identified over a one-year period at a single institution. All (n = 6) patients were undergoing neurosurgical procedures. Four patients required surgical retrieval of the catheter fragments. No patient experienced log-term neurological sequelae., Discussion: From these experiences, the following risks factors for catheter rupture are identified: 1) intentional or accidental retraction of the catheter through the needle during placement; 2) faulty use of the guidewire; or 3) use of excessive force during removal of the catheter. Methods to prevent such complications are suggested, including minimal use, or complete avoidance of a guidewire.

Purpose: To describe an episode of acute jugular venous desaturation during intraoperative rupture of a cerebral aneurysm., Clinical Features: A 57-yr-old patient was scheduled for clipping of a large unruptured basilar tip aneurysm. Abrupt bulging of the brain was observed after bone flap removal, but before dura was opened. This was associated with concurrent development of systemic hypertension to 200/120 mmHg and jugular venous bulb (S(jv)O(2)) desaturation to 13%. Rupture of aneurysm was confirmed by frank blood in cerebrospinal fluid drainage from the lumbar subarachnoid catheter., Conclusions: Abrupt S(jv)O(2) desaturation prior to dural opening may suggest an acute increase in intracranial pressure, which in our case followed aneurysmal rupture; the systemic response to increased intracranial pressure (Cushing's response) may be ineffective in maintaining cerebral perfusion.

Purpose: We describe cerebral hyperemia and impaired cerebral autoregulation documented with transcranial Doppler (TCD) ultrasonography in an adult patient with diabetic ketoacidosis (DKA) and sepsis presenting for surgery., Clinical Features: Middle cerebral artery flow velocity was increased relative to PaCO(2) (Vmca 52 cm.sec(-1); PaCO(2) 22 mmHg) and the autoregulatory index (ARI) was 0 prior to surgery. Twenty hours after admission and treatment, cerebral hyperemia resolved (Vmca 52 cm.sec(-1) ; PaCO(2) 35 mmHg) and cerebral autoregulation returned to normal (ARI 0.91)., Conclusion: To our knowledge, this is the first description of impaired cerebral autoregulation in adult DKA. Our observations suggest a relationship between cerebral hyperemia and impaired cerebral autoregulation in DKA.

Purpose: The effects of anesthetic management on blood flow to the optic nerve have not been well-studied. The ophthalmic artery provides the majority of the blood supply to the optic nerve via several smaller branches. Retinal blood flow has been shown to react to carbon dioxide (CO(2)) similar to intracranial vessels, but insufficient data exist for the ophthalmic artery. The purpose of this study is to examine the CO(2)-reactivity of the ophthalmic artery., Methods: Eight healthy awake subjects aged 28 to 50 yr were tested for CO(2)-reactivity in the ophthalmic artery using transcranial Doppler (TCD) insonation of blood flow velocity (V(op)), while simultaneously recording the V(op) of the middle cerebral artery (V(mca)) as an internal control. V(op) and V(mca) recordings were made under hypocapnic, normocapnic and hypercapnic conditions., Results: The CO(2)-reactivity slope of V(mca) was 3.27% per mmHg PaCO(2). From normocapnia to hypercapnia, V(op) did not change significantly (mean +/- SD, 18 +/- 4 cm*sec(-1) to 18 +/- 6 cm*sec(-1)), (end-tidal CO(2), etCO(2), = 43 +/- 5 mmHg to 53 +/- 4 mmHg, respectively). In contrast, V(op) increased significantly under hypocapnic conditions (etCO(2) = 26 +/- 4 mmHg) to 25 +/- 5 cm*sec(-1) (P < 0.05). The CO(2)-reactivity slope of V(op) from normocapnia to hypocapnia was 2.57% per mmHg., Conclusions: This study demonstrates that V(op) increases with hypocapnia, but is unaffected by hypercapnia. The anastomoses of the ophthalmic artery with the external carotid artery, which displays a relatively fixed resistance, may account for these findings.

Cerebral venous oxygen desaturation may occur when hyperventilation is employed during neurosurgical procedures. In this study, we examined the effect of arterial hyperoxia (PaO2 > 200 mmHg) on jugular bulb venous oxygen tension (PjvO2), saturation (SjvO2) and content (CjvO2) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (FIO2) was varied to give four different levels of arterial oxygen tension (PaO2 100-200, 201-300, 301-400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO2(25) and 30 mmHg). In five patients, a transcranial Doppler probe was used to insonate the middle cerebral artery throughout the study period. Regression lines were constructed for each patient for the PjvO2, SjvO2 and the corresponding PaO2 for both levels of PaCO2 (all PjvO2-PaO2 and SjvO2-PaO2 regression lines r2 > 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2 and CjvO2 at PaO2 of 100, 250 and 400 mmHg, at each level of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia increased PjvO2 (from 27.6 +/- 1.1 mmHg at PaO2 of 100 mmHg to 30.6 +/- 1.4 and 33.6 +/- 1.8 mmHg at PaO2 of 250 and 400 mmHg respectively) and SjvO2 (from 54 +/- 3% at PaO2 of 100 mmHg to 60 +/- 3 and 65 +/- 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2 and PjvO2 at a PaCO2 of 30 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Intraoperative monitoring of somatosensory-evoked potentials is a routine procedure. To determine the depressant effect of nitrous oxide relative to isoflurane, the authors recorded the scalp, cervical and brachial plexus-evoked responses to stimulation of the median nerve under different anaesthetic conditions. Eight subjects, age 35 +/- 6 (SD) yr, weight 68 +/- 12 kg, were studied. Following recording of awake control responses, anaesthesia was induced with thiopentone 5 mg.kg-1 and fentanyl 3 micrograms.kg-1 and was followed by succinylcholine 1 mg.kg-1. During normocapnia and normothermia, and with a maintenance infusion of fentanyl 3 micrograms.kg-1.hr-1, evoked potential recording was repeated under three different anaesthetic conditions; 0.6 MAC nitrous oxide, 0.6 MAC nitrous oxide +/- 0.6 MAC isoflurane, and 0.6 MAC isoflurane. Among the anesthetic conditions, the combination of nitrous oxide-isoflurane had the most depressant effect on the cortical amplitude (67 +/- 4% reduction, P < 0.05). Nitrous oxide decreased the cortical amplitude more than an equipotent dose of isoflurane (60 +/- 4% vs 48 +/- 7%, P < 0.05). The latency was unchanged by nitrous oxide, but increased slightly by isoflurane and isoflurane-nitrous oxide anaesthesia (1.0 and 0.9 msec respectively, P < 0.05). We conclude that somatosensory-evoked potential monitoring is feasible both during nitrous oxide anaesthesia and isoflurane anaesthesia, but the cortical amplitude is better preserved during 0.6 MAC of isoflurane alone relative to 0.6 MAC of nitrous oxide alone. The depressant effect is maximal during nitrous oxide-isoflurane anaesthesia but less than the predicted additive effect.

The purpose of this study was to compare and assess the ability of two different evoked potential (EP) modalities, median nerve somatosensory evoked potentials (SSEP) and brainstem auditory evoked potentials (BAEP) in monitoring for cerebral ischaemia and in predicting neurological outcome during posterior fossa aneurysm surgery. During 70 procedures, patients were monitored with both SSEP and BAEP. Temporary occlusion of an artery was used in 52 patients and permanent occlusion in 21 patients. A change was defined as a greater than 50% decrease in amplitude and/or an increase in latency greater than 1 msec of the N20 (cortical waveform) for SSEP monitoring and of the fifth peak for BAEP monitoring. Neurological assessment of the patient was performed immediately on emergence, after 24 hr and at the time of discharge. In total, 14 patients had an SSEP change which predicted a neurological deficit in eight patients (57%). Ten patients had a change in BAEP; six had a neurological deficit (60%). Five patients had a change in both, two had a deficit (40%). The incidence of false negative results (a neurological deficit but no EP change) for both modalities was 20% (SSEP 47%, BAEP 60%). The incidence of false positive results (an EP change but no deficit) was 13% overall (SSEP 11%, BAEP 7%). All patients who had a permanent EP change developed a neurological deficit. We did not find a difference in the ability of SSEP compared with BAEP in predicting neurological deficits but, using both modalities, the incidence of false negative results was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

In 17 healthy patients undergoing O2.N2O.isoflurane anaesthesia, following atracurium or vecuronium administration, we compared simultaneous integrated evoked electromyograms (IEEMGs) during spontaneous recovery of the adductor digiti minimi (ADM) and orbicularis oris (OOM) muscle groups in response to train-of-four (TOF) stimulation of the ulnar and facial nerves, respectively. In all patients, the onset of neuromuscular recovery occurred first in the OOM. The time required to recover to a T4/T1 = 0.70 +/- 0.01 (SD) was earlier in the OOM compared with the ADM muscles in both the atracurium (33.4 +/- 5 vs 46.5 +/- 8, P less than 0.005) and vecuronium (46.5 +/- 12 vs 60.3 +/- 20, P less than 0.005) groups. When the OOM attained a T4/T1 = 0.70 +/- 0.01, the simultaneous T4/T1 in the ADM was 0.29 +/- 0.15 (P less than 0.05) in the atracurium group and 0.41 +/- 0.16 (P less than 0.01) in the vecuronium group. We conclude that (1) the facial muscles (OOM) recover earlier than the hypothenar muscles (ADM) and (2) an EMG T4/T1 = 0.70 in the facial muscles may not indicate adequate recovery of neuromuscular function.

In six healthy volunteers, integrated evoked electromyography (IEEMG) measured in response to ulnar nerve stimulation was correlated with respiratory function-tidal volume (VT), forced vital capacity (FVC), forced expiratory volume in one second (FEV1), maximum negative inspiratory pressure (NIP), hand grip (HG) and head-lift during steady-state infusion of subparalytic doses of atracurium. Studies were carried out at train-of-four T4/T1 = 0.2 and T4/T1 = 0.6. When T4/T1 = 0.2, all subjects had difficulty with swallowing and phonation, none could sustain any head-lift and HG was 26 per cent of control. However, VT was normal, FVC was 80 per cent, FEV1 was 82 per cent, and NIP was 50 per cent of control. AT T4/T1 = 0.6, all assessments of peripheral strength were normal, and all respiratory measurements were not significantly different from control, except for NIP which was 73 per cent of control (P less than 0.05). We conclude that an IEEMG of 0.6, recorded from the hypothenar muscles, in unanaesthetized subjects is consistent with near normal respiratory function.

Plasma epinephrine (PE), plasma norepinephrine (PNE), plasma renin activity (PRA), mean arterial pressure (MAP) and heart rate (HR) were measured before, during and after induced hypotension in two groups of patients undergoing cerebral aneurysm surgery. In Group I isoflurane was used to maintain anaesthesia and induce hypotension. Mean PE fell significantly during hypotension and remained reduced after hypotension, mean PNE remained unchanged, while mean PRA rose slightly but not significantly during hypotension, falling again after hypotension. In Group II halothane was used to maintain anaesthesia and sodium nitroprusside to induce hypotension. During anaesthesia and surgical stimulation PNE and PRA were significantly greater compared to Group I. Mean PE, PNE and PRA all rose during hypotension and remained elevated after hypotension. The rise in PNE and PRA was statistically significant. After hypotension the MAP in Group II was significantly higher when compared to Group I. There was no significant change in HR during the study in either group. In conclusion, isoflurane-induced hypotension with isoflurane anaesthesia unlike sodium nitroprusside-induced hypotension with halothane anaesthesia attenuated the stress response.

Intraoperative monitoring of sensory-evoked potential has been found to be useful in many areas, particularly during scoliosis surgery and neurovascular surgery. However, it remains a complicated technique, devoid of simple interpretation and as such cannot be considered a routine clinical monitor except in large centres with special expertise. Increase in utilization must await improvement in technique and development of strict criteria for interpretation.

In order to determine the cerebral protective effects of an intravenous bolus of 5 mg.kg-1 of lidocaine, the left middle cerebral artery (MCA) was transorbitally occluded in 19 cats. Ten animals received the lidocaine bolus and nine a similar volume of saline immediately before MCA occlusion. Somatosensory evoked potentials (SEP) were recorded before and after the lidocaine bolus as well as continually after MCA occlusion. After six hours of vessel occlusion and without reperfusion, the animals were sacrificed and the brains fixed for histology. Prior to MCA occlusion, lidocaine caused a statistically significant (p less than 0.01) reduction in the amplitude of the major cortical component of the SEP (10 +/- 1.2 microV vs 6.0 +/- 1.3 microV). Latency was unchanged. In the lidocaine group, SEP's persisted in 40 per cent immediately following occlusion whereas they disappeared in all of the control animals (p less than 0.05). Gradual recovery occurred in both groups and there were no differences at the end of the experiment although the amplitudes tended to be greater in the lidocaine group. There were no statistically significant differences in the histological size or severity of the infarcts between the groups. Although infarct size was not reduced, transient sparing of the SEP suggests that further studies of lidocaine by continuous infusion in models of temporary focal cerebral ischaemia may be warranted.

The effect of mannitol on serum and urine electrolytes and osmolality was investigated intraoperatively in neurosurgical patients. Patients in Group A (n = 7) received 1 gm . kg-1 of 20 per cent mannitol ("low"-dose) and in Group B, (n = 7) 2 gm . kg-1 ("high"-dose). There was a significant decrease in serum sodium and bicarbonate, and a significant increase in serum osmolality in both groups after mannitol administration. The decrease in serum sodium and the increase in serum osmolality were significantly greater in patients receiving the larger dose of mannitol. The infusion of low-dose mannitol resulted in a slight decrease in serum potassium. In contrast, after high-dose mannitol there was a significant rise in serum potassium reaching a maximum mean increase of 1.5 mmol . l-1. Urine electrolyte concentration and osmolality showed a similar decrease in both groups. The significant changes that occurred with the administration of mannitol were of short duration in these patients with normal cardiac and renal function. The clinically most important change is the increase in serum potassium with high-dose mannitol. The exact mechanism of this increase remains unclear.

Moyamoya disease is a rare neurovascular condition that affects both children and adults. Increasingly these patients present for surgical management to improve the cerebral circulation since medical therapy is essentially ineffective. Because of the precarious cerebral circulation, these patients represent an anaesthetic challenge. In this report we review the pathophysiology of moyamoya disease, summarize our experience with seven patients and discuss the anaesthetic management.

We evaluated the effects of isoflurane anaesthesia and induced hypotension in 33 neurosurgical patients by electrocardiographic monitoring and serial cardiac enzyme measurements. An electrocardiogram (ECG) and serum enzymes were obtained preoperatively, intraoperatively and postoperatively in the recovery room and for three consecutive days. ECG leads II, V1 and V5 were monitored continuously during anaesthesia. Patients who had had a subarachnoid haemorrhage and a high incidence of abnormal preoperative ECG (42 per cent). Ten patients developed ECG changes intraoperatively, but these changes were unrelated to isoflurane-induced hypotension. Fifty-three per cent of patients developed an abnormal postoperative ECG. These abnormalities consisted mostly of nonspecific ST segment or T wave changes. At no time was there an elevation in cardiac enzyme activity. We found that nonspecific ECG changes are relatively common in patients undergoing vascular neurosurgical procedures. There was no enzymatic evidence of myocardial infarction and we can only speculate that these ECG changes are related to intracranial surgical manipulation.