Scalp nerve blocks decrease the severity of pain after craniotomy.

UNLABELLED: Up to 80% of patients report moderate to severe pain after craniotomy. In this study, we assessed the efficacy of scalp block for decreasing postoperative pain in brain surgery. Thirty patients scheduled for supratentorial craniotomy were enrolled. They were randomly divided into two groups: Ropivacaine (scalp block with 20 mL of ropivacaine 0.75%) and Saline (scalp block with 20 mL of saline 0.9%). Anesthesia was standardized. The scalp block was performed after skin closure and before awakening. Postoperative pain was assessed at 4, 8, 12, 16, 20, 24, and 48 h by using a 10-cm visual analog scale. Analgesia was provided with sub- cutaneous codeine as requested by the patient. Average visual analog scale scores were higher in the Saline group as compared with Ropivacaine (3.7 +/- 2.4 vs 2.0 +/- 1.6; P = 0.036). The total dose of codeine did not differ, nor did the duration of time before the first dose of codeine was required in the Ropivacaine (571 +/- 765 min) versus Saline (319 +/- 409 min; P = 0.17) group. In conclusion, we found that postoperative scalp block decreases the severity of pain after craniotomy and that this effect is long lasting, possibly through a preemptive mechanism. IMPLICATIONS: Up to 80% of patients report moderate to severe pain after craniotomy. This randomized double-blinded study demonstrated that ropivacaine scalp block decreases the severity of pain after supratentorial craniotomy.

Voluntary hyperventilation before a rapid-sequence induction of anesthesia does not decrease postintubation PaCO2.

UNLABELLED: To prevent hypercapnia, voluntary hyperventilation is recommended for patients with increased intracranial pressure before the induction of general anesthesia. We sought to determine whether this maneuver results in a lower PaCO2 than breathing 3 min of oxygen 100% by face mask (preoxygenation) after intubation. Thirty patients requiring general anesthesia were randomly assigned to breathe either 3 min of oxygen 100% by face mask (Group P) or 1 min of oxygen 100% followed by 2 min of voluntary hyperventilation with oxygen 100% (Group H). All patients received a standard rapid-sequence induction of anesthesia followed by a 90-s period of apnea. Patients were then tracheally intubated and mechanically ventilated. Five arterial blood gas samples were taken: with room air, after preoxygenation or hyperventilation, after 60 and 90 s of apnea, and after tracheal intubation. Voluntary hyperventilation decreased PaCO2 before rapid-sequence induction (hyperventilation, 30.0 +/- 3.5 mm Hg versus preoxygenation, 37.9 +/- 5.2 mm Hg; P < 0.0001), but after 60 s of apnea, both groups had similar PaCO2 (hyperventilation, 36.1 +/- 3.3 mm Hg versus preoxygenation, 35.6 +/- 3.4 mm Hg; P = 0.673), and no benefit was found after intubation (hyperventilation, 40.5 +/- 3.9 mm Hg versus preoxygenation, 41.4 +/- 2.7 mm Hg; P = 0.603). We conclude that voluntary hyperventilation before rapid-sequence induction does not provide protection against potential hypercapnia during intubation. IMPLICATIONS: Voluntary hyperventilation before anesthesia induction is recommended for patients with increased intracranial pressure to prevent hypercapnia. This randomized, prospective study demonstrated that this maneuver does not result in a lower postintubation PaCO2 than standard preoxygenation.

[Is isoflurane a calcium antagonist?]. / L'isoflurane est-il un antagoniste du calcium?

The vasodilating and myocardial depressant effects of isoflurane have been allocated to calcium channel blockade. The present study aimed to test this hypothesis by assessing the effect of isoflurane on the contractile response to potassium stimulation of vascular smooth muscle. Seventy two left anterior descending and circumflex coronary artery rings were removed in twelve dogs and mounted in organ chambers filled with Krebs-Ringer bicarbonate solution and aerated with 95% O2-5% CO2. Rings were pretreated with either 3.8% isoflurane (2.5 MAC in the dog) or 10(-8) mol.l-1 nifedipine, a calcium entry blocker. They were stimulated by addition of 10 to 150 mmol.l-1 potassium chloride. At 70 mmol.l-1 K+, the tension generated by the untreated rings was 119 +/- 4.25% of control, while in the isoflurane treated group the tension was 99 +/- 2.4% of control. In the opposite, the tension was 25 +/- 7.11% in the nifedipine treated rings. Likewise, when isoflurane was added to rings preconstricted with 40 mmol.l-1 potassium chloride, no relaxation occurred, while nifedipine produced relaxation. Isoflurane, unlike nifedipine, had a weak effect on ring tension. The calcium-entry blockade effect of isoflurane appeared weak, dose-dependent and virtually absent at clinical concentrations. Therefore, the vasodilation seen with clinical concentrations of isoflurane is mediated by mechanisms other than calcium-entry blockade.