Jennifer Greger

Continuous Lateral Sciatic Blocks for Acute Postoperative Pain Management after Major Ankle and Foot Surgery

We developed a continuous lateral sciatic nerve infusion technique for postoperative analgesia. Methods: A 10-cm insulated Tuohy needle connected to a nerve stimulator was introduced posteriorly between the biceps femoris and vastus lateralis groove 10 cm cephalad from the tip of the patella. After proper positioning of the insulated needle, a 20-gauge catheter was placed in proximity to the sciatic nerve. Results: Continuous lateral sciatic infusion of 0.2% ropivacaine was associated with a significant reduction of morphine consumption by 29% and 62% during postoperative days one and two, respectively, in patients who underwent open reduction and internal fixation of the ankle. Conclusion: Continuous lateral sciatic infusion of 0.2% ropivacaine represents an alternative for acute postoperative pain control after major ankle and foot surgery.

Continuous posterior lumbar plexus block for acute postoperative pain control in young children.

A 60-yr-old man, 160 cm tall, weighing 75 kg, with American Society of Anesthesiologists physical status class II, was admitted for elective right shoulder surgery. His medical history was unremarkable except for recent mild diabetes with no related neuropathy, controlled by diet and glimepiride. Physical examination results were unremarkable, and the results of laboratory studies were all within normal limits, including preoperative glycemia and chest x-ray. He agreed to undergo a combination of regional and general anesthesia. Hydroxyzine, 100 mg, was administered 2 h preoperatively. After application of routine monitors, intravenous access was secured. He was positioned supine with the head turned to the contralateral side, and the right side of the neck was prepared as a sterile field. The elbow was flexed, with the forearm lying on the patient’s abdomen. Thereafter, interscalene brachial plexus block was performed as described by Winnie but using a nerve stimulator to ascertain that the needle’s tip was in the brachial plexus. The plexus was located with a nerve stimulator (Stimuplex HNS 11; B/Braun, Melsungen, Germany) and an insulated needle, 25 mm long with a short 30° bevel (Stimuplex, B/Braun). Three attempts at needle insertion were required to achieve an appropriate motor response: the brachial plexus was first located using a high current intensity (2 mA; 0.1 ms and 1 Hz), and then it was decreased to 0.5 mA to refine the approach. After obtaining a motor response of the deltoid muscle, a mixture of 30 ml ropivacaine, 0.75%, and 75 g clonidine was injected. No blood could be aspirated, and the patient reported neither pain nor paresthesia during the procedure, although phrenic nerve stimulation was transiently observed. After 20 min, profound surgical anesthesia was established on C5–C7 dermatomes. Then, general anesthesia was induced with 2 mg midazolam, 100 g fentanyl, 200 mg propofol, and 30 mg atracurium to facilitate tracheal intubation. General anesthesia was maintained with 1–2% sevoflurane and 50% nitrous oxide, and the patient underwent a right rotator cuff repair via a deltopectoral approach. He was placed in a “beach chair” position with his head turned the opposite direction. Vital signs and standard parameters remained stable throughout the 2-h procedure. At the end of surgery, the trachea was extubated, and the patient was observed for 1 h in the postanesthesia care unit. He did not report any pain. Vital signs and postoperative glycemia were normal. The interscalene brachial plexus blockade was still effective. Postoperative analgesia consisted of regular administration of a combination of propacetamol and nefopam intravenously. The patient was discharged to the ward. Postoperative follow-up was unremarkable. Ten days later, the patient was readmitted to the hospital because of increasing shortness of breath. A chest roentgenogram revealed marked elevation of the right hemidiaphragm when compared with the preoperative chest film. No signs of infection or other disorders were shown on the film. This pattern was suggestive of acquired phrenic nerve palsy. Because the moderate difficulty in breathing persisted despite physiotherapy, a complete checkup was made 3 months after the block. A new chest x-ray confirmed that the elevation of the right hemidiaphragm was unchanged and revealed atelectasis limited to the lower part of the right lung field, probably related to the right ventilatory deficit. No movement of the hemidiaphragm was observed during fluoroscopy, and paradoxical motion was shown by sniffing maneuver. Pulmonary function tests showed mild restrictive lung disease: vital capacity, forced expiratory volume in 1 s, forced vital capacity, and total lung capacity were respectively reduced to 89, 79, 88, and 76% of predicted values. By contrast, peak expiratory flow rate, arterial oxygen tension (PaO2), and arterial carbon dioxide tension (PaCO2) were in the normal range. Computed tomography and nuclear magnetic resonance scans of the neck and thorax were also normal. A definitive diagnosis of phrenic nerve dysfunction as the cause of hemidiaphragm paralysis was obtained by electromyography using phrenic nerve stimulation in the neck and the measurements of phrenic nerve latencies and conduction velocities. Stimulating electrodes were placed over the phrenic nerve in the supraclavicular fossa. The compound action potential of the hemidiaphragm was recorded using surface electrodes placed on the anterolateral aspect of the chest in the seventh intercostal space in the anterior axillary line. Results showed the absence of a right phrenic nerve compound action potential, whereas the left phrenic nerve conduction velocity was normal, suggesting that the right phrenic nerve was completely interrupted or significantly demyelinated. Although this examination failed to identify the mechanism or the precise location of the lesion, it was useful in confirming the lack of electromyographic pattern of diffuse neuropathy. One year after surgery, the patient still reported exertional dyspnea with no functional improvement.

What Has Happened to Evidence-based Medicine?

To the Editor:—We read with great interest the article by Petersen et al., which demonstrated the expected clinical response to the three anesthetic agents studied. An increase in arterial pressure may result in an increase in the cerebral perfusion pressure and reduce reflex cerebral vasodilatation, potentially resulting in reduced intracranial pressure. We note that the mean arterial pressures in the propofol group were substantially higher than in the two inhalation groups, both before and after hyperventilation. The propofol group was shown to have both a lower measured intracranial pressure and subjective surgical estimation of brain swelling at craniotomy. The influence of the potentially higher perfusion pressure on these findings in this group cannot be estimated from the study. Was this relationship between mean arterial pressure and intracranial pressure examined by the authors, and if so, could they comment on its possible significance? Robert A. Fry, M.B., Ch.B.* Nigel N. Robertson, M.B., Ch.B. *Auckland Hospital, Auckland New Zealand. robf@adhb.govt