Endovascular Nuances in Management of Multiple Intracranial Aneurysms.

BACKGROUND: Endovascular treatment of aneurysm is the accepted standard of treatment. Multiple intracranial aneurysms are frequently detected due to advances in imaging. OBJECTIVE: The purpose of this study was to determine aneurysm properties, management strategies, and outcome of patients with multiple intracranial aneurysms managed by endovascular approach. MATERIALS AND METHODS: Data of all patients with multiple intracranial aneurysms who were managed at our institute over a period of 1 year were retrospectively studied. Data of 20 consecutive patients with single aneurysm who were endovascularly managed during the same study period were also collected. Patient demographics, intraprocedural radiation exposure, hardware used, and clinical and angiographic outcome at discharge were analyzed. RESULTS: A total of 112 patients with intracranial aneurysm were managed during the study period, of which 11 patients had multiple intracranial aneurysms, with a total of 23 aneurysms. Incidence was more among females (63.6%). Proximal of multiple aneurysms ruptured more commonly (63.6%), and internal carotid artery (ICA) bifurcation was the most common site (45.4%). Of the 23 aneurysms, 18 were coiled. Seven patients had good outcome and it was found to be influenced by preoperative Hunt and Hess scale. Based on Raymond-Roy grading, 17 of 18 aneurysms (94.4%) were completely coiled; angiographic outcome was comparable in both the groups. Patients with multiple aneurysm had statistically significant high radiation exposure (4.5 vs 3.8 m SV) as compared to patients with single aneurysm (P < 0.05), but had low stochastic effect. In patients with aneurysm involving different arterial compartment, 66.2% required change of microcatheter. CONCLUSION: Single-stage treatment of multiple aneurysm can be achieved with good outcome. Even though radiation exposure is high while treating multiple aneurysm as compared to single aneurysm cases, its stochastic risks are low.

Quadriplegia in a child following adenotonsillectomy.

Neurological deterioration in a child following routine surgery, although rare, has potentially life threatening consequences. We report the case of a child who, following adentonsillectomy, developed quadriplegia and acute respiratory distress due to previously undetected atlanto-axial instability. Patients with atlanto-axial instability often have mild or non-specific symptoms, despite severe cervical cord compression. Subtle manifestations may be ignored or attributed to other disease processes, which render patients with undiagnosed atlanto-axial instability at risk of serious neurological injury during general anaesthesia, particularly at the time of laryngoscopy and tracheal intubation.

Intra procedure rupture of intracranial aneurysm during endovascular coiling: neurosurgeons' experience and review of the literature.

OBJECTIVE: The aim of this study was to determine the incidence, risk factors and outcome of intra procedure rupture (IPR) during endovascular coiling of intracranial aneurysms, a neurosurgeons' experience. MATERIALS AND METHODS: The frequency of IPR was studied in 168 aneurysms treated by endovascular coiling in 150 consecutive patients. Aneurysm size, morphology, history of previous subarachnoid hemorrhage (ruptured) and timing of treatment after subarachnoid hemorrhage were the data collected for comparison. RESULTS: Procedure-related rupture during endovascular coiling occurred in five (2.97%) of the 168 aneurysms treated. IPR was the cause for 1.78% treatment-related deaths. Small aneurysm size was the major risk factor for IPR in this series (P < 0.001). CONCLUSIONS: In this study, the frequency of IPR was similar to the reported frequency in the procedures performed by neurointerventionists.

Bladder distension: An unusual cause of reflux of blood and hemodynamic changes (autonomic dysreflexia) during endovascular coiling.

Autonomic dysreflexia due to distended bladder is well known. Reflux of blood during endovascular procedure is also a common observation. It happens due to difference in pressure gradient between arterial pressure and that of infusing solution. Generally it happens when the infusion bottle is empty or the pressure in infusion bottles fall. We present an uncommon situation where distended bladder mechanically resulted in reflux of blood into endovascular catheters as well as alteration in hemodynamic parameters. Both settled once the bladder was empty.

Incidence and pattern of intraoperative hemodynamic response to endoscopic third ventriculostomy.

BACKGROUND: In patients undergoing endoscopic third ventriculostomy (ETV), various cardiovascular changes occur in the intraoperative period. AIM: We tried to determine a pattern in these changes and their relation to different surgical steps. MATERIALS AND METHODS: A total of 260 patients were studied over a period of six years. Heart rate and mean arterial pressures were recorded before introduction of the endoscope and thereafter at various stages of the operation. RESULTS: Tachycardia was the predominant observed abnormality in 20% of patients, occurring mostly during manipulations and irrigation in the third ventricle (TV). Bradycardia was seen in 12% of patients, more often during fenestration of the floor of the third ventricle. CONCLUSIONS: Tachycardia observed during ETV may be related to hypothalamic stimulation or a rise in intracranial pressure and bradycardia may be due to stimulation of the hypothalamus or the third cranial nerve. Anticipation of these cardiovascular changes during the relevant steps of the operation can help in taking appropriate corrective action, thus preventing potentially serious complications of ETV.

Effects of intrathecal ketamine added to bupivacaine for spinal anaesthesia.

We prospectively studied 30 healthy female patients undergoing intracavitory brachytherapy applicator insertion for carcinoma of the cervix under spinal anaesthesia. Patients were randomly allocated to receive either intrathecal bupivacaine 10 mg alone or bupivacaine 7.5 mg combined with preservative-free ketamine 25 mg. Spinal block onset, maximum sensory level, duration of blockade, haemodynamic variables, postoperative analgesic requirements and adverse events were recorded. Onset of sensory and motor block and duration of spinal analgesia were comparable between groups. Duration of motor blockade was shorter (p = 0.0416) and requirement for intravenous fluids in the peri-operative period was less (p = 0.0159) in the ketamine group. Significantly more patients in the ketamine group had adverse events, such as sedation, dizziness, nystagmus, 'strange feelings' and postoperative nausea and vomiting. Although the addition of ketamine to spinal bupivacaine had local anaesthetic sparing effects, it did not provide extended postoperative analgesia or decrease the postoperative analgesic requirements. Moreover, the central adverse effects of ketamine limit its spinal application.

Pretreatment with dexmedetomidine: altered indices of anesthetic depth for halothane in the neuraxis of cats.

UNLABELLED: The sedative and anesthetic-sparing ability of the alpha2-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 microg/kg p.o.). In both groups, four indices of anesthetic depth--minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to noxious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG isoelectricity)--were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3.14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis. IMPLICATIONS: The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.

In vivo effects of dexmedetomidine on laser-Doppler flow and pial arteriolar diameter.

BACKGROUND: The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter. METHODS: Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min). RESULTS: Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored. CONCLUSIONS: These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.

Desflurane attenuates the somatosympathetic reflex in rats.

Arterial blood pressure and heart rate changes after afferent somatic sensory nerve stimulation are termed the "somatosympathetic reflex" (SSR). Inhibition of the SSR may partially represent an antinociceptive action. This investigation examined the actions of the volatile anesthetic, desflurane, on the SSR evoked by peripheral nerve stimulation. Rats anesthetized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) were mechanically ventilated and cannulated with arterial and venous catheters for monitoring arterial pressure and for fluid administration, respectively. The sciatic (n = 7) or tibial (n = 6) nerves were isolated and stimulated at one, two, and four times the voltage threshold required to elicit a change in systemic hemodynamics. These cardiovascular responses were recorded before, during, and after varying concentrations of desflurane, 1.8% (0.25 minimum alveolar anesthetic concentration [MAC]), 3.6% (0.5 MAC), 7.2% (1.0 MAC), and 10.8% (1.5 MAC). Desflurane decreased arterial pressure at 1.0 and 1.5 MAC and heart rate (at more than 0.5 MAC) compared to baseline levels. Tibial nerve stimulation decreased mean arterial pressure (MAP) with no consistent changes in heart rate. Desflurane significantly attenuated this depressor response to tibial nerve stimulation (MAP decrease: control; -20 +/- 2 mm Hg versus 1.0 MAC desflurane; -6 +/- 4 mm Hg). The increases in MAP after sciatic nerve stimulation were also significantly inhibited by increasing concentrations of desflurane. At more than 0.5 MAC desflurane, the pressor response to sciatic nerve stimulation was significantly converted to a depressor response in four of seven rats (MAP: control; increase 24 +/- 2 mm Hg versus 1.0 MAC desflurane; decrease -2 +/- 4 mm Hg). Sciatic nerve stimulation also elicited increases in heart rate which were significantly attenuated by desflurane (control; 37 +/- 6 bpm versus 1.5 MAC desflurane; 0 +/- 2 bpm). These findings demonstrate that desflurane produces dose-dependent cardiovascular depression in rats and, despite previous reports of sympathoexcitation, desflurane significantly attenuated both excitatory and inhibitory types of SSR. The results of this study also support a potential antinociceptive action for this anesthetic.

Posterior fossa surgery in postshunt endocarditis patients: some anesthetic issues.

A patient with an intracranial fourth ventricular cyst developed right heart endocarditis from an infected ventriculoatrial shunt inserted previously. Investigation revealed pneumonic involvement of the right lung, moderate tricuspid regurgitation, mild pulmonary artery hypertension, and a large right atrial vegetation. The shunt was removed and treatment of endocarditis started, before undertaking excision of the cyst under general anesthesia. During the operation there was a sudden deterioration in the patient's condition rapidly leading to death. Clinical features suggested intraoperative pulmonary embolism; both venous air embolism and a dislodged atrial vegetation were considered. However, in the absence of specific monitoring equipment and autopsy, the actual cause could not be ascertained. This clinical report highlights the anesthetic problems related to posterior fossa surgery in patients with right-sided endocarditis and suggests some possible management strategies.

Postblock epidural hematoma causing paraplegia. Case report.

BACKGROUND AND OBJECTIVES: An elderly man with no obvious preexisting coagulation disorder had paraplegia following epidural block for transurethral prostatectomy that was later found to be due to a large epidural hematoma requiring surgical decompression of the spinal cord. METHODS: There was a delay in starting treatment since the cause was not initially suspected. RESULTS: The patient did not improve much after the operation. CONCLUSIONS: The anesthesiologist should be alert to the possibility of epidural hematoma forming in otherwise normal patients to avoid such unfavorable outcomes.