A 32-Year-Old Man Diagnosed with Type II Brugada Syndrome on Preoperative Electrocardiogram 1 Week Before Elective Tympanoplasty.

BACKGROUND Brugada syndrome is a potentially fatal cardiac arrhythmia characterized by incomplete right bundle-branch block (RBB) and characteristic ST-segment elevation in the anterior electrocardiogram (ECG) leads. This report is of a case of type 2 Brugada syndrome, and discusses the importance of preoperative history and ECG evaluation. CASE REPORT A 32-year-old man was scheduled for tympanoplasty. His preoperative ECG revealed saddleback-type J waves in V2 (>2 mm) and ST increase (>1 mm) detected 1 week before elective surgery, but the ECG 1 year before showed normal. He had no notable past history. Anesthesia was induced with remifentanil and propofol, and maintained with sevoflurane in combination with remifentanil. Routine monitoring of vital signs was supplemented with V2 monitoring on the ECG. The heart rate was maintained at above 60 beats/min using ephedrine. The course of the operation was uneventful. CONCLUSIONS We managed anesthesia for a patient with a type 2 Brugada syndrome ECG without events, probably because he had no notable past history such as syncope. Type 2 and type 3 Brugada syndrome ECGs are difficult to recognize, and patients with them are considered to be less risky than a patient with a type I ECG. However, as Brugada syndrome ECG is dynamic and changeable, a type 2 or 3 Brugada syndrome ECG can change to a type I ECG under some conditions, and thus should not be overlooked, and the patient's past history or symptoms, such as syncope, should be carefully investigated.

Unusually large ephedrine-induced blood pressure increases due to cardiac sympathetic denervation supersensitivity in a patient with Parkinson's disease.

BACKGROUND: Parkinson's disease (PD) patients often suffer from cardiac sympathetic denervation, a hallmark of which is orthostatic hypotension. Denervation supersensitivity to sympathomimetic drugs is also seen in such patients, and this phenomenon is important and can be sometimes dangerous. CASE PRESENTATION: A 65-year-old male underwent gastrojejunostomy. The patient had severe PD and did not exhibit metaiodobenzylguanidine (MIBG) accumulation in his heart, which was indicative of cardiac sympathetic nerve denervation. When 8 mg of ephedrine was administered intravenously, an unexpectedly large increase in blood pressure was observed. The phenomenon recurred when 4 mg of ephedrine was administered again, and nicardipine was required to suppress the patient's blood pressure. CONCLUSIONS: Denervation supersensitivity is not as well recognized as other complications seen in PD patients, but anesthesiologists should be aware of it because sympathomimetic drugs can have excessively strong effects in patients with the condition.

Preoperative Prevalence of J-Wave Syndrome Electrocardiographic Patterns and Their Association With Perioperative Cardiac Events.

OBJECTIVE: To evaluate the preoperative prevalence of each type of J-wave syndrome electrocardiographic pattern and its association with perioperative cardiac events. DESIGN: Retrospective study. SETTING: Single hospital university study. PARTICIPANTS: The study evaluated 930 patients who underwent gynecologic, abdominal, neurosurgical, orthopedic, and urologic surgeries. INTERVENTIONS: Preoperative standard 12-lead electrocardiogram (ECG) monitoring was performed, and each type of J-wave syndrome ECG pattern-types 1, 2, and 3 and Brugada syndrome-type-was evaluated. Incidence of perioperative cardiac events was investigated up to 1 year postoperatively using an electronic medical record system. MEASUREMENTS AND MAIN RESULTS: Data from 789 patients were included in the final study. Of these, 16 patients (2.0%) had J-wave syndrome: 7 patients (0.9%) had type-1 patterns; 5 patients (0.6%) had type-2 patterns; 2 patients (0.3%) had type-3 patterns; and 2 patients (0.3%) had Brugada syndrome-type ECG patterns. A J-point elevation≥0.2 mV, which is considered to be more dangerous, was found in only 2 patients with Brugada syndrome-type ECG patterns, both of whom suffered perioperative lethal arrhythmias. CONCLUSION: Patients with J-wave syndrome ECG patterns, even dangerous patterns, are not necessarily associated with a higher risk of perioperative cardiac events. However, Brugada syndrome type ECG patterns should be carefully monitored.

Transient lower limb pain following accidental thoracic subarachnoid insertion of an epidural catheter.

Transient sensory disturbances, including dysesthesia or neurologic deficits in the lower extremities or buttocks have been described as complications of neuraxial anesthesia. We report a case of transient lower limb pain following the accidental placement of an epidural catheter into the thoracic subarachnoid space. A 31-year-old woman was scheduled to undergo laparoscopic myomectomy. An epidural catheter was accidentally inserted subarachnoid at the T12-L1 intervertebral space with a 2-ml test dose of 2% lidocaine, and was promptly removed. Fulgurant pain and allodynia extending over the L2-5 areas of the left lower limb and buttock started immediately postoperatively. We treated the persistent pain in our patient with epidural infusion of local anesthetics and steroids during her hospital stay, and with carbamazepine and a tricyclic antidepressant after her discharge from the hospital. All signs of allodynia had disappeared on postoperative day 25. Sagittal and axial T2-weighted magnetic resonance imaging (MRI) at the Th12 level revealed a small high-intensity area without mass effect in the ipsilateral dorsal column. The patient's clinical course and MRI diagnosis suggested the inhibition of descending inhibitory pathways resulting from a lesion of the spinal cord as the possible etiology of the transient lower limb pain and allodynia.

Suppression of the descending inhibitory pathway by continuous thoracic intrathecal lidocaine infusion reduces the thermal threshold of the tail-flick response in rats.

PURPOSE: For the suppression of descending inhibitory pathways in animals, single-dose lidocaine blockade is reversible and causes less damage than chronic spinal cord injury, decerebration, and cold blockade of the spinal cord. However, single-dose blockade has a variable onset and is relatively short-lived. To surmount these disadvantages, we devised a continuous thoracic intrathecal lidocaine infusion and evaluated its effects in rats. METHODS: Rats were administered continuous intrathecal infusions of 0, 0.25%, 0.5%, and 1% lidocaine at 10 &gml.h(-1) following a 10-&gml bolus. The effects of the continuous thoracic blockade on tail-flick (TF) latency (estimated by the percent maximum possible effect [%MPE]) and on the release of neurotransmitters in the cerebrospinal fluid (CSF) were evaluated. RESULTS: Continuous thoracic blockade with 0.5% and 1% lidocaine infusion reversibly shortened TF latency (%MPE, -22.0 +/- 11.0 % and -21.2 +/- 4.6 %, respectively, versus baseline; P < 0.05) during drug infusion. Compared with normal saline, thoracic intrathecal infusion of lidocaine significantly lowered norepinephrine and serotonin concentrations in the CSF at 1 h of infusion (P = 0.02 for both). CONCLUSION: Continuous thoracic blockade by local anesthetic resulted in reversible suppression of descending inhibitory pathways for varying durations. Such blockade may provide further information regarding nociceptive transmission and the mechanisms of antinociception in animals.

The effect of Sub-MAC anesthesia and the radiation setting on repeated tail flick testing in rats.

The tail flick (TF) response is regarded as a spinal reflex that is influenced by supraspinal structures. The TF test using radiant heat is the most common way to assess pain perception; however, there are few reports dealing with the heat source's properties and score consistency. This study examined the usefulness of light anesthesia for suppressing supraspinal signals and the effects of radiant heat on skin temperature during TF testing. The fluctuations of TF latency over one hour were evaluated while the rats were given oxygen and 0%, 0.5%, 1.0%, or 1.5% isoflurane. The stimulator's infrared radiant (IR) power flux was measured over time, and the tail skin surface temperature was predicted using a non-linear regression equation. TF latencies were measured at various heat source intensities, and response temperatures were estimated. Inhalation anesthesia suppressed the TF reflex according to the inspiratory concentration of the volatile anesthetic. IR power fluxes reached constant power 2.5 s after the stimulator was turned on, and the predicted skin temperature depended on the maximum IR power flux of the IR intensity and the radiation time. One percent isoflurane inhalation and an IR20 heat intensity (which was 161.5 mW/cm(2) and resulted in a skin temperature of 65 degrees C after 10 s of radiation) provided reliable TF latencies on repeated TF testing. Given these results, it can be concluded that the stimulator setting influenced TF latency, and that the inhalation of light anesthesia provided consistent scores on repeated TF testing.