Mazen A. Maktabi

A prospective, comparative trial of three anesthetics for elective supratentorial craniotomy : propofol/fentanyl, isoflurane/nitrous oxide, and fentanyl/nitrous oxide

Background:Different anesthetic agents have different effects on cerebrovascular physiology. However, the importance of these differences In neuroanesthetic practice are unclear. In an effort to determine whether important clinical differences are present, the authors compared three anesthetic techniques in 121 adults undergoing elective surgical removal of a supratentorial, intracranial mass lesion. Methods:Patients were assigned randomly to one of three groups. In group 1 (n=40), anesthesia was induced with propofol and maintained with fentanyl (≊10 µg/kg load, 2-3 µg · kg-1 · h-1 infusion) and propofol (50-300 µg · kg-1 · mln-1). In group 2 (n=40), anesthesia was induced with thiopental and maintained with isoflurane and nitrous oxide. Up to 2 µg/kg fentanyl was given after replacement of the bone flap. In group 3 (n=41), anesthesia was induced with thiopental and maintained with fentanyl (≊10 µg/kg load, 2-3 µg · kg-1 · h1 infusion), nitrous oxide, and low-dose Isoflurane, if required. Blood pressure, heart rate, expired gas concentrations, and ventilatory parameters were recorded automatically in all patients. Epidural intracranial pressure (ICP) was measured via the first burr hole, brain swelling was rated at the time of dural opening, and emergence was monitored closely. Preoperative computed tomography or magnetic resonance imaging scans were evaluated, and pre- and postoperative neurologic exams were performed by a neurosurgeon unaware of group assignments. Total hospital stay (days) and total hospital cost (exclusive of physician charges) also were reviewed. Results:During induction, higher heart rates were seen in isoflurane/nitrous oxide patients, whereas mean arterial pressure was ≊10 mmHg less during the maintenance phase (compared with both other groups). Otherwise, there were few intergroup hemodynamic differences. While there were no clinically important intergroup differences in mean ICP (±SD)—group 1, ICP=12 ± 7 mmHg; group 2,15 ± 12 mmHg; group 3, ICP=11 ± 8 mmHg—more isoflurane/nitrous oxide patients (nine, group 2) had an ICP £24 mmHg than in the other groups (two each). Emergence was, overall, more rapid with fentanyl/nitrous oxide. For example, the median time until the patient could be awakened by quiet verbal command, e.g., “Open your eyes,” was 5 min, versus 10 min in the other groups. There were no relationships between ICP and any measurement of emergence (e.g., time to response to commands). Seven of 41 (17%) fentanyl/nitrous oxide patients vomited In the early postoperative period, compared with only 1 of 40 (2.5%) of those given propofol/fentanyl and 2 of 40 (5%) receiving isoflurane/nitrous oxide (P=0.03). There were no differences in the incidence of new postoperative deficits, total hospital stay, or cost. Conclusions:Although there are modest differences among the three tested anesthetics, short-term outcome was not affected. These results indicate that, despite their respective cerebrovascular effects, all of the anesthetic regimens used were acceptable in these patients undergoing elective surgery.

Comparison of Remifentanil and Fentanyl in Patients Undergoing Craniotomy for Supratentorial Space-occupying Lesions

BackgroundRemifentanil hydrochloride is an ultra-short-acting, esterase-metabolized micro-opioid receptor agonist. This study compared the use of remifentanil or fentanyl during elective supratentorial craniotomy for space-occupying lesions.MethodsSixty-three adults gave written informed consent for

Endoscopic Study of Mechanisms of Failure of Endotracheal Tube Advancement into the Trachea during Awake Fiberoptic Orotracheal Intubation

Background: Advancing the endotracheal tube (ETT) over a flexible bronchoscope (FB) during awake fiberoptic orotracheal intubation is often impeded. The goal of this study was to identify the sites and mechanisms that inhibit the passing of the ETT into the trachea. Methods: Forty-five consenting patients underwent a clinically indicated awake fiberoptic orotracheal intubation. After topical anesthesia, nerve block, or both, an awake fiberoptic orotracheal intubation was performed. The placement of the FB and advancement of the ETT over the FB were videotaped using a second nasally inserted FB. An otolaryngologist later reviewed the videotaped data. Results: The right arytenoid or the interarytenoid soft tissues inhibited advancement of the ETT in 42 and 11% of all patients, respectively. In all cases in which the FB was located on the right side of the larynx, failure of ETT advancement almost always occurred at the right arytenoid. Withdrawing the ETT and rotating it 90° counterclockwise resulted in successful intubation on the second, third, and fourth attempts in 26.6, 20, and 0.7% of patients, respectively. Conclusion: The right arytenoid frequently inhibits advancement of the ETT over the FB into the trachea during awake fiberoptic orotracheal intubation. The FB position in the larynx before tube advancement and the orientation of the ETT are relevant factors in failure of advancement of the ETT into the trachea. The authors recommend positioning the FB in the center of the larynx and orienting the bevel of the ETT to face posteriorly during the first attempt at intubation.

Manual In-line Stabilization Increases Pressures Applied by the Laryngoscope Blade during Direct Laryngoscopy and Orotracheal Intubation

Background:Manual in-line stabilization (MILS) is recommended during direct laryngoscopy and intubation in patients with known or suspected cervical spine instability. Because MILS impairs glottic visualization, the authors hypothesized that anesthesiologists would apply greater pressure during intubations with MILS than without. Methods:Nine anesthetized and pharmacologically paralyzed patients underwent two sequential laryngoscopies and intubations, one with MILS and one without, in random order. A transducer array along a Macintosh 3 laryngoscope blade continuously measured applied pressures, and glottic view was characterized. Results:With MILS, glottic visualization was worse in six patients, and intubation failure occurred in two of these six patients. Maximum laryngoscope pressure at best glottic view was greater with MILS than without (717 ± 339 mmHg vs. 363 ± 121 mmHg, respectively; n = 8; P = 0.023). Other measures of pressure application also indicated comparable increases with MILS. Conclusion:Pressures applied to airway tissues by the laryngoscope blade are secondarily transmitted to the cervical spine and result in cranio-cervical motion. In the presence of cervical instability, impaired glottic visualization and secondary increases in pressure application with MILS have the potential to increase pathologic cranio-cervical motion.

The Dose-related Effects of Nitric Oxide Synthase Inhibition on Cerebral Blood Flow during Isoflurane and Pentobarbital Anesthesia

Background:Recent work in animals suggests that nitric oxide may play a role In the cerebral blood flow (CBF) changes produced by anesthetics, particularly the vasodilation seen with volatile anesthetics. It is not clear, however, whether nitric oxide causes the flow increase or simply plays some constitutive role. To distinguish between these possibilities, we studied the dose-related effects of nitric oxide synthase inhibition in rabbits with varying baseline CBFs, produced by anesthesia with isoflurane, low-dose pentobarbital, or high-dose pentobarbital. Methods:New Zealand White rabbits were anesthetized with 1 MAC isoflurane, low-dose pentobarbital (50-mg/kg load, 7.5-mg kg-1.h-1 infusion), or high-dose pentobarbital (50-mg/kg load, 20-mg kg-1.h-1 deep burst-suppression on the electroencephalogram), and prepared for the measurement of CBF using radioactive microspheres. The confluence of sinuses was also exposed to permit sampling of cerebral venous blood and the determination of cerebral metabolic rate for O2 (CMRo2). Normocapnia and normothermia were maintained throughout. After baseline measurements, animals were sequentially given a cumulative total of 3, 13, and 43 mg/kg intravenous Nω--nitro-L-arginine methyl ester (l.-NAME), an inhibitor of nitric oxide synthase. CBF and CMRo2 were recorded =10 min after each dose. Results:L-NAME produced a dose-related reduction in CBF in all three anesthetic groups. Statistical examination indicated that the dose response curves were parallel. For example, in isoflurane-anesthetized rabbits, CBF decreased from 77 ± 19 to 47 ± 11 ml.100 g-1.min-1 after the 43 mg/kg L-NAME, whereas in high-dose pentobarbital animals, CBF decreased from 42 ± 15 to 26 ± 8 ml 100 g-1 min-1 (all values mean ± SD). Decreases in CMUo2 did not quite achieve significance (P = 0.08), and the CBF/CMKO2 ratio decreased in all animals, suggesting that the CBF reductions were due primarily to direct vasoconstriction. There were no electroencephalographic changes. In separate groups of Isoflurane-anesthetized rabbits given 3 mg/kg L-NAME, treatment with 300 mg/kg L-arginine partially reversed the decreases in CBF. By contrast, the effects of 43 mg/kg L-NAME were not reversible with 430 mg/kg L-arginine. Conclusions:Although L-NAME reduced CBF in all three anesthetic conditions, it did not alter the relative differences among them: CBF in the presence of isoflurane remained much higher than that seen with the barbiturates. This suggests that nitric oxide may not the primary mediator of anesthetic CBF effects, but rather acts to influence background vascular tone in these anesthetized animals.

Is Routine Endotracheal Intubation as Safe as We Think or Wish

EVERY year, millions (tens of millions?) of patients undergo laryngoscopy and tracheal intubation as part of their routine anesthetic care. Although this method was only rarely used in our practice before the 1960s, it is now almost as routine as placing a peripheral intravenous catheter. A great deal of attention is devoted to airway management in general (particularly the patient with a difficult airway), but we rarely give much thought to the consequence of intubation in patients with complete, normal (easy) airways. In this issue of ANESTHESIOLOGY, Tanaka et al. describe measurable changes in the larynx following routine endotracheal intubations. The changes consisted of increased airflow resistance that was attributed to intraoperative swelling of the laryngeal soft tissues in patients who were intubated. Such postoperative laryngeal changes were absent in the patients who received a laryngeal mask airway for anesthesia. It is tempting to dismiss the findings of this study as intuitively predictable or trivial. However, we believe that the findings represent the less severe end of the spectrum of airway injuries caused by tracheal intubation. The findings of Tanaka et al. confirm our long-held belief that even routine tracheal intubation produces changes in the airway. These changes may vary from those that are very mild (detectable only with elaborate methods, such as in Tanaka’s study) to the very serious. For example, Domino et al. analyzed the claims of airway injuries in the American Society of Anesthesiologists closed claims project. Of the 266 claims related to airway injury, 87 involved the larynx, with the most common lesions being vocal cord paralysis, granulomas, arytenoid dislocation, and hematomas. However, “80% of laryngeal injuries were associated with routine (nondifficult) tracheal intubation. . .,” and only 17 of these cases were associated with a difficult intubation. Airway injuries placed fourth (6%) behind three other major types of injuries: death (32%), spinal cord or peripheral nerve damage (16%), and brain damage (12%). Others have observed serious laryngeal injuries (e.g., vocal cord paralysis, arytenoid cartilage subluxation, laryngeal granulomas, and scars) following short-term intubation and anesthesia. Paulsen et al. compiled a list of several reports of arytenoid cartilage subluxation. In most of these reports, intubation was performed without apparent difficulty and the patients were intubated for a short period of time. These findings suggest that laryngeal damage was related to intubation and not to duration of surgery. Although there are some differences in opinion with regard to general risk factors, several factors were suggested for arytenoids subluxation, including laryngomalacia, renal insufficiency, acromegaly, chronic glucocorticoid intake, and rheumatoid arthritis. An important clinical sign of potential postoperative laryngeal injury is voice dysfunction, namely, hoarseness. The most common cause for postoperative hoarseness in patients undergoing procedures that do not involve the head and neck is swelling of the vocal cords. Recent evidence by Mencke et al. suggests that the quality of intubation contributes to laryngeal morbidity. Specifically, intubating conditions that are associated with various degrees of coughing, resistance to laryngoscope blade insertion (difficult laryngoscopy because of the patient being light/inadequately paralyzed), and limb movement are associated with a greater incidence of postoperative hoarseness and laryngeal injuries. Most of the laryngeal trauma occurred in patients who received no neuromuscular blockers to facilitate routine endotracheal intubations. Mencke et al. concluded that the use of neuromuscular blockers in the sequence of induction drugs is associated with better intubating conditions and less postoperative hoarseness and laryngeal injury. It seems that under suboptimal intubating conditions, even the mildest body movement may lead to mechanical trauma caused by the laryngoscope or endotracheal tube, resulting in laryngeal or tracheal injury. We find it very interesting that that by taking a simple measure, such as adding neuromuscular blockers at induction, the incidence of postoperative hoarseness dramatically dropped. Although Menke’s study focused on the role of intubating conditions in postoperative laryngeal morbidity, the incidence of hoarseness or laryngeal dysfunction following routine tracheal intubation is not clear. Previous research by Jones et al. found that 54 of 167 studied patients had hoarseness following short-term intubation. In five of these patients, hoarseness lasted for periods ranging between 9 and 99 days. Kark et al. reported hoarseness that lasted for more than 6 months in 3% of women undergoing mastectomies. The figures presented by Domino, Mencke, Jones, and Kark are This Editorial View accompanies the following article: Tanaka A, Isono S, Ishikawa T, Sato J, Nishino T: Laryngeal resistance before and after minor surgery: Endotracheal tube versus laryngeal mask airway. ANESTHESIOLOGY 2003; 99:252–8.

Comparison of nitroprusside, nitroglycerin, and deep isoflurane anesthesia for induced hypotension.

Three methods of inducing hypotension were studied for their effects on the cardiovascular system and intrapulmonary shunting. Thirty patients were anesthetized with isoflurane in 70% N2O to a total of 1.25 to 1.3 MAC. Patients were divided into three groups of 10 each on the basis of the drug used to induce hypotension; sodium nitroprusside (SNP), nitroglycerin (NTG), or deep isoflurane anesthesia (ISF). Cardiac index was significantly decreased by NTG and ISF at a mean arterial blood pressure of 40 mm Hg compared to SNP (P less than 0.05). Systemic vascular resistance was decreased in all groups. Mixed venous oxygen content was significantly decreased from control in the NTG and ISF groups. There was no difference between the groups in arterial and mixed venous O2 content. Intrapulmonary shunting decreased with induction and, in the NTG and SNP groups, increased slightly but not significantly with induction of hypotension. Our data do not show a clear superiority of any agent over the other to induce hypotension, although SNP and perhaps ISF appear to be better than NTG to induce hypotension.

Epidural Meperidine-bupivacaine for Obstetric Analgesia

In 13 full-term primipara in active labor an initial single dose of preservative-free meperidine (100 mg) diluted in 10 ml of saline was injected epidurally (L2-3). In another 13 full-term parturients in active labor, 10 ml of bupivacaine 0.25% was used. Pain was scored by the linear analog scale. Onset of analgesia was 5.3 ± 2.8 minutes following administration of meperidine, and 12.9 ± 6.9 minutes following bupivacaine (p < 0.011. Pain score decreased to 0 in 12 of 13 patients following meperidine administration and in six of 13 patients following bupivacaine (p < 0.01). Satisfactory analgesia lasted 160.8 ± 90.3 minutes following meperidine, and 103.5 ± 42 minutes following bupivacaine administration (p < 0.01). Subsequent supplementation by intermittent doses of 10 ml of bupivacaine 0.25% was more effective and less frequent following meperidine than following bupivacaine administration. Maternal sedation, nausea, and itching occurred frequently following administration of epidural meperidine, whereas hypotension, numbness, and motor dysfunction followed bupivacaine. In neither group was significant respiratory depression observed. All parturients delivered vaginally, 288 ± 212.6 minutes following meperidine and 348 ± 195.8 minutes following bupivacaine administration (p > 0.05); the neonates showed normal Apgar scores and neurobehavioral responses. Epidural meperidine, supplemented by subsequent bupivacaine as indicated, provides maternal sedation and satisfactory analgesia, and it diminishes the requirements of bupivacaine supplementation. The technique is advantageous in the parturient primipara.

Angiotensin II Contributes to Cerebral Vasodilatation During Hypoxia in the Rabbit

BACKGROUND and Purpose Hypoxia increases cerebral blood flow (CBF). Hypoxia also exerts a major influence on the renin-angiotensin system. In addition to the circulating renin-angiotensin system, a local renin-angiotensin system appears to be present in the brain, and angiotensin II receptors have been identified in cerebral blood vessels. In this study we tested the hypothesis that endogenous angiotensin II attenuates dilatation of the cerebral vessels during hypoxia. METHODS Pentobarbital-anesthetized rabbits were prepared for measurement of blood flow (microspheres) and assigned to one of two groups: in group 1 (n = 11), rabbits were subjected to 30 minutes of stable hypoxia (PaO2 = 34 +/- 1 mm Hg, mean +/- SD) followed by 15 minutes of reoxygenation (PaO2 = 177 to 200 mm Hg). Blood flow was measured four times: under control conditions, after 15 and 30 minutes of hypoxia, and after 15 minutes of reoxygenation. This was a control group to characterize changes in CBF during hypoxia. In group 2 (n = 11), blood flow was measured as in the previous group except that an infusion of the angiotensin II receptor antagonist saralasin (1 microgram.kg-1.min-1 IV) was started with the onset of hypoxia and continued through reoxygenation to the end of the experiment. The goal of this group was to examine whether endogenous activation of receptors for angiotensin II influences increases in CBF during hypoxia. In a separate series of experiments we examined the influence of the angiotensin-converting enzyme (ACE) inhibitor captopril on the hypoxic response. Thus, in one group of rabbits we measured CBF in the same manner as in group 1 (n = 13). In another group of rabbits we also measured blood flow as in group 1 except that rabbits received 10 mg/kg of the ACE inhibitor captopril before the control measurement (n = 11). We tested for significant differences between groups using two-way ANOVA. RESULTS Under control conditions, CBF was similar in all groups and averaged 53 +/- 15 mL.min-1.100 g-1. During hypoxia, CBF increased to a greater extent in the absence versus the presence of saralasin (95 +/- 31 and 104 +/- 30 mL.min-1.100 g-1 versus 72 +/- 24 and 71 +/- 25 mL.min-1.100 g-1, respectively; P = .003). Increase in CBF during hypoxia was also significantly greater in the animals that did not receive captopril versus those that were treated with captopril (100 +/- 24 and 89 +/- 16 mL.min-1.100 g-1 versus 72 +/- 16 and 73 +/- 17 mL.min-1.100 g-1). To rule out the possibility that saralasin produced non-specific attenuation of cerebral vasodilatation, we tested the influence of hypercapnia on CBF in the absence and presence of saralasin. During normocapnia, CBF values were not significantly different in the absence and presence of saralasin (57 +/- 17 and 64 +/- 6 mL.min-1.100 g-1, respectively; P > .05). Hypercapnia increased CBF similarly in the absence and presence of saralasin (81 +/- 22 and 91 +/- 19 mL.min-1.100 g-1; PaCO2 = 61 +/- 2 and 60 +/- 2 mm Hg, respectively; P > .05). CONCLUSIONS Because the ACE inhibitor captopril and the angiotensin II receptor blocker saralasin attenuated increased in CBF during hypoxia, the findings suggest that endogenous release of angiotensin II contributes to the increase in CBF during hypoxia.

Nicardipine HCL: clinical experience in patients undergoing anaesthesia for intracranial aneurysm clipping

Previous studies have reported haemodynamic interactions between dihydropyridine calcium antagonists and general anaesthesia. During anaesthesia for intracranial aneurysm surgery, we prospectively compared haemodynamic values obtained from 13 patients being treated with nicardipine HCl (0.15 mg · kg-1 · hr-1 IV) for cerebral vasospasm against values obtained from 11 untreated controls. Prior to induction of anaesthesia, nicardipine-treated patients had significantly elevated mean ± SD cardiac index (5.67 ± 1.30 vs 3.99 ± 0.73 L · min-1 · m-1) while MAP (86 ± 10 vs 99 ± 14 mmHg) and systemic vascular resistance (647 ± 227 vs 1141 ± 404 dynes · sec-1 · cm-1) were reduced. Heart rate, CVP, and PACWP were similar between groups. Anaesthesia induction and tracheal intubation resulted in similar haemodynamic values between groups with the exception of CVP (10 ± 5 vs 5 ± 2 mmHg) and PACWP (15 ± 5 vs 8 ± 3 mmHg) which were elevated in the nicardipine group (P < 0.01). Mannitol infusion and deliberate hypotension resulted in nearly identical haemodynamic responses in both groups. Nicardipine-treated patients required more intravenous fluids during the operative procedure (2.4 ± 0.3 L vs l.5 ± 0.4 L, P < 0.05) and were less likely to require isofturane supplementation to morphine sulphatel nitrous oxide anaesthesia (P < 0.01). In summary, our experience with nicardipine HCl revealed no major untowardRésuméDes études antérieures ont rapporté des intéractions hémodynamiques entre les antagonistes du calcium dihydropyridine et ľanesthésie générale. Durant ľanesthésie pour résection ďun anéurysme intracrânien, on a comparé ďune façon prospective les valeurs hémodynamiques obtenues chez treize patients ayant été traités avec la nicardipine HCl (0.15mg·kg-1hre-1 IV) pour vasospasme cérébral avec des valeurs obtenues chez onze patients contrôle non traités. Avant ľinduction, les patients traités à la nicardipine avaient une élévation significative de la valeur moyenne ± SD de ľindex cardiaque (5.67 ± 1.30 vs 3.99 ±0.73 L·min·-1m-1) alors que la pression artérielle moyenne (86 ± 10 vs 99 ± 14 mmHg) et la résistance vasculaire systémique (647 ± 227 vs 1141 ± 404 dynes·sec-1 ·cm-1) étaient diminuées. La fréquence cardiaque, la pression veineuse centrale et la pression bloquée de ľartère pulmonaire étaient similaires dans les deux groupes. Ľinduction de ľanesthésie et ľintubation ont produit des valeurs hémodynamiques similaires entre les groupes à ľexception de la pression veineuse centrale (10 ± 5 vs 4 ± 2 mmHg) et la pression bloquée de ľartère pulmonaire (15 ± 5 vs 8 ± 3 mmHg) qui étaient élevées dans le groupe nicardipine (P < 0.01). La perfusion de mannitol et ľhypotension contrôlée ont amené des réponses hémodynamiques quasi identiques dans les deux groupes. Les patients traités à la nicardipine ont requis plus de liquide lors de la procédure chirurgicale (2.4 ± 0.3 Lvs 1.5 ± 0.4 L, P < 0.05) et avaient tendance à recevoir moins ďisoflurane supplémentaire lors ďune anesthésie au sulfate de morphinelprotoxyde ďazote (P < 0.01). En résumé, notre expérience avec HCl nicardipine n’a pas démontré ďeffets secondaires sur la stabilité hémodynamique peropératoire malgré la continuation de la thérapie antispasmodique avec ce vasodilatateur.