Paradoxical vocal fold motion masquerading as post-anesthetic respiratory distress: A case report.

BACKGROUND: Functional vocal cord disorders can be a differential diagnosis for postoperative upper airway obstruction requiring urgent intervention. However, this may be unfamiliar to anesthesiologists who would favor inappropriate airway intervention and increased morbidity. CASE SUMMARY: A 61-year-old woman underwent cervical laminectomy, followed by laparoscopic cholecystectomy 10 mo later. Despite adequate reversal of neuromuscular blockade, the patient experienced repetitive respiratory difficulty with inspiratory stridor after extubation. After the second operation, the patient was diagnosed with paradoxical vocal fold motion (PVFM) by an otolaryngologist based on the clinical features and fiberoptic bronchoscopy results, and the patient was successfully treated. CONCLUSION: PVFM should be considered a differential diagnosis if a patient presents with stridor after general anesthesia.

Prophylactic antibiotics induce early postcraniotomy seizures in neurosurgery patients: A case series.

RATIONALE: Antibiotics can cause central nervous system disturbances, manifesting as dizziness, confusion, headache, and seizures. Seizures due to antibiotic administration are related to increased excitatory neurotransmission because antibiotics act as competitive antagonists of the γ-aminobutyric acid type A receptor. PATIENT CONCERNS AND CLINICAL FINDINGS: All 5 patients, comprising 4 females and one male and aged 45 to 72 years, underwent open craniotomy with additional surgical maneuvers according to their specific disease. All patients presented American Society of Anesthesiologists Physical Status grades 1 to 2. There were no specific underlying diseases, except hepatitis C and hypertension. However, seizures developed sequentially in the 5 patients after neurosurgery. DIAGNOSES, INTERVENTIONS, AND OUTCOMES: Early postcraniotomy seizures (PCS) developed in the patients after neurosurgery. Prophylactic antibiotics were administered in all cases to prevent infection due to open craniotomy. This included the administration of 10 g and 2 g of an antibiotic (cefotiam HCL; Jetiam Intravenous Injection 1g®) an hour before the surgery in the ward and half an hour before the surgery in the operating room, respectively. After surgery, cefotiam HCL 2 g was administered in all patients on the day of surgery. Five patients had myoclonic seizure or generalized tonic-clonic seizure several times at emergence or in the intensive care unit. LESSONS: Early PCS occurred in every patient when an overdose of the prophylactic antibiotic was administered. This report showed that the preoperative prophylactic antibiotic cefotiam administered in double doses evoked early PCS within a few hours of drug administration. Furthermore, such experiences caution that preoperative intravenous cephalosporins, including cefotiam, should be administered carefully in open craniotomy.

Effects of Blood Transfusion on Hepatic Ischemia-Reperfusion Injury-Induced Renal Tubular Injury.

OBJECTIVES: Hepatic ischemia-reperfusion injury and transfusion of red blood cells in liver surgery are wellknown risk factors to induce acute tubular injury. Transfusion of stored red blood cells may affect hepatic ischemia-reperfusion injury-induced acute tubular injury. Here, we hypothesized whether preischemic (due to increased severity of hepatic injury) and postischemic (due to renal uptake of free heme and iron) transfusion of stored red blood cells may potentiate acute tubular injury in rats subjected to hepatic ischemia-reperfusion injury. MATERIALS AND METHODS: Sprague Dawley rats (n = 24) were divided into 4 groups: sham operation (sham group), hepatic ischemia-reperfusion injury only (injury-only group), red blood cell transfusion before hepatic ischemia-reperfusion injury (preinjury transfusion group), and red blood celltransfusion after hepatic ischemia-reperfusion injury (postinjury transfusion group). Partial hepatic ischemia was induced for 90 minutes, with reperfusion allowed for 12 hours. Hepatic and renal tubular injury markers, renal mRNA levels of oxidant stress markers, and inflammatory markers were assessed. Renal cortex samples were examined under hematoxylin and eosin staining for tubular histopathologic score and immunohistochemical staining forinflammatory cells. RESULTS: With regard to hepatic and renal tubular injury markers, serum alanine aminotransferase, serum urea nitrogen, and histopathologic scores were increased in the preinjury and postinjury transfusion groups versus injury-only group, with moderate to strong correlation between alanine aminotransferase and tubular injury markers. Renal oxidative stress markers (heme oxygenase-1 and neutrophil gelatinaseassociated lipocalin) were correlated with increased alanine aminotransferase, with upregulation of oxidant stress markers in the preinjury transfusion group versus sham group (all markers), as well as in the injury-only and postinjury transfusion groups (heme oxygenase-1 only). We observed no changes in renal inflammatory responses among the groups. CONCLUSIONS: Preischemic transfusion potentiated acute tubular injury without triggering renal inflammatory responses. Exacerbation of hepatic injury may induce acute tubular injury via renal oxidant stress.

General anesthesia for patient with Fahr's syndrome: A case report.

RATIONALE: Fahr's syndrome (FS) is a rare neurological and psychiatric disorder characterized by bilateral brain calcifications when a secondary cause of the calcification is found. PATIENT CONCERNS: A 53-year-old female patient diagnosed with FS for laminectomy because of ossification of posterior longitudinal ligament. She had a history of generalized tonic-clonic (GTC) seizure and medication with anticonvulsant drugs. She had gait disturbance, spasticity, bradykinesia, and diffuse calcifications in the basal ganglia, thalamus, cerebellum, and cerebral hemispheres on the brain computed tomography. On the preoperative examination, the serum and ionized calcium (Ca) were decreased to 3.7 and 2.22 mg/dL. Hypomagnesemia is combined with hypocalcemia. Furthermore, the level of parathyroid hormone was decreased to 2.18 pg/mL. DIAGNOSES: Due to the radiologic findings and laboratory test results, she was diagnosed with FS with primary hypoparathyroidism. INTERVENTIONS: The Ca and magnesium (Mg) had been corrected before surgery but the electrolytes revealed low level at the intraoperative period. The 300 mg of calcium chloride was administered at 2 times and 1200 mg of it were infused for 1 hour during intraoperative periods. In addition, total 4 g of Mg sulfate intravenously administered. We used rocuronium as a neuromuscular block and checked neuromuscular function by train-of-four monitoring. OUTCOMES: Residual neuromuscular blockade was reversed with pyridostigmine and her muscle power completely recovered. The patient was extubated successfully and no unpredictable events occurred. On the day following transfer, serum electrolytes remained low, and although Ca was continuously supplied, serum Ca did not recover to a normal level. The patient was medicated with anticonvulsant drugs but experienced GTC seizure 2 weeks after surgery. LESSONS: We presume that the pathophysiology of FS was related to primary hypoparathyroidism and hypomagnesemia. FS raises concerns associated with neuromuscular problems, spasticity, and seizure, and concerns of hypotension, heart failure, cardiac arrhythmia, and cerebrovascular attack during perioperative periods, among anesthesiologists because of hypocalcemia and vessel calcification. During the perioperative period, Ca levels should be closely monitored, and titrated Ca replacement therapy is recommended. The simultaneous correction of hypomagnesemia is of considerable importance when correcting hypocalcemia.

Hyperventilation Syndrome and Sustained Hyperchloremia After Kidney Transplant: Time-Sequence Swing of Acid-Base Interpretation.

An interaction between regained renal function in a transplanted kidney and hyperventilation syndrome may interfere with correct diagnosis of acid-base status in patients with preoperative nongap acidosis. Here, we present a patient with glomerular nephritis and hyperchloremia who underwent kidney transplant. Progressively increasing bicarbonate reabsorption by the renal graft, which thereby changed the arterial carbon dioxide tension-to-bicarbonate ratio, resulted in a time-sequence swing of an acid-base interpretation despite persistent mixed respiratory alkalosis due to hyperventilation syndrome and nongap metabolic acidosis due to preexisting hyperchloremia. Specifically, the sequence was mixed primary metabolic acidosis and primary respiratory acidosis immediately after surgery, primary metabolic acidosis and secondary respiratory alkalosis on postoperative days 1 and 2, mixed primary hyperchloremic metabolic acidosis and primary respiratory alkalosis on postoperative day 3, and finally primary respiratory alkalosis and secondary hyperchloremic metabolic acidosis on postoperative day 7. This swing in the acid-base interpretation indicates that the acid-base imbalance described here does not fit the empirical relationship for calculating the expected bicarbonate or carbon dioxide tension value, suggesting that "correct" interpretation of acid-base status may not lead to "correct" diagnosis of acid-base status. It should be remembered that not every acid-base imbalance fits the empirical relationship.

Preischemic transfusion of old packed RBCs exacerbates early-phase warm hepatic ischemia reperfusion injury in rats.

BACKGROUND: Hepatic innate immune cells are considered to play a central role in the early phase of hepatic ischemia reperfusion (IR) injury. Transfusion of old red blood cells (RBCs) is known to prime immune cells, and transfusion before IR may exacerbate liver injury because of the expected hyperresponsiveness of immune cells. MATERIALS AND METHODS: Twenty-four Sprague-Dawley rats were divided into four groups: sham operation (Sham); hepatic IR only (IR Control); and two transfusion groups, preischemic (Pre-T) and postischemic (Post-T), in which allogeneic RBCs stored for 2 weeks were transfused before hepatic IR or after reperfusion, respectively. Partial hepatic ischemia was induced for 90 min, and reperfusion was allowed for 120 min. Serum alanine transaminase levels, area of necrosis, and apoptotic cells were then assessed. Inflammatory (tumor necrosis factor alpha, interleukin 1 beta [IL-1ß], IL-6, IL-10, and cyclooxygenase 2) and oxidative mediators (heme oxygenase 1, superoxide dismutase, and glutathione peroxidase 1) were assessed for elucidating the relevant mechanisms underlying the hepatic injury. RESULTS: Pre-T, but not Post-T, showed increased serum alanine transaminase levels than IR Control (P < 0.05). Area of necrosis was more severe in Pre-T than in IR Control or Post-T (P < 0.01), and apoptotic cells were also more abundant in Pre-T than in IR Control (P < 0.01). tumor necrosis factor alpha and IL-6 levels were higher in Pre-T than in IR Control or Post-T (P < 0.05), with no significant difference in cytoprotective protein levels. CONCLUSIONS: Preischemic transfusion of old RBCs aggravated hepatic injury. Inflammatory cytokines seemed to play a crucial role in liver injury exacerbation. Our results indicate that transfusion before hepatic ischemia may be detrimental.

Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury.

BACKGROUND: Superoxide, nitric oxide (NO), and peroxynitrite are important mediators in the pathogenesis of ischemia-reperfusion (I/R) injury. We tested the renoprotective effects of allopurinol (ALP), a xanthine oxidase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), and 5,10,15,20-tetrakis (N-methyl-4-pyridyl) porphyrinato iron (III) (FeTMPyP) by selective inhibition of superoxide, NO, and peroxynitrite, respectively. METHODS: Male Sprague-Dawley rats were randomly assigned to 5 groups (n = 6 per group). Group 1 was a sham-operated group. Group 2 was the renal I/R group (30-minute ischemia followed by 24-hour reperfusion). Rats in groups 3, 4, and 5 received ALP, L-NAME, or FeTMPyP, respectively, at 5 minutes before the reperfusion. Serum creatinine (Cr), blood urea nitrogen (BUN), renal tissue malondialdehyde, superoxide dismutase, histological changes, apoptosis, and monocyte infiltration were evaluated. In addition, the combined treatment with ALP and L-NAME was compared with FeTMPyP in a second independent experiment. RESULTS: The administration of ALP, L-NAME, and FeTMPyP diminished the increase in Cr (P = .0066 for all) and BUN (P = .0066 for ALP; and P = .013 for L-NAME) induced by I/R injury and decreased the histological damage (P = .0066 for all). In addition, ALP, L-NAME, and FeTMPyP attenuated the oxidative stress response as determined by a decrease in malondialdehyde level (P = .0066 for all), apoptotic renal tubular cells (P = .0066 for all), and monocyte infiltration (P = .0066 for all). The combined treatment of ALP and L-NAME decreased Cr and BUN levels to a greater degree than FeTMPyP (P = .016 for Cr; P = .0079 for BUN). CONCLUSIONS: Superoxide, NO, and peroxynitrite are involved in renal I/R injury. The reduction of peroxynitrite formation, via inhibition of superoxide or NO, or the induction of peroxynitrite decomposition may be beneficial in renal I/R injury.

Optimal effect-site concentration of remifentanil for inhibiting response to laryngeal mask airway removal during emergence.

PURPOSE: This randomized, controlled, double-blind study was designed to determine the optimal dose of remifentanil for preventing complications associated with the removal of a laryngeal mask airway (LMA) without delaying emergence. MATERIALS AND METHODS: This study randomly assigned 128 patients to remifentanil effect-site concentrations (Ce) of 0 ng/mL (group R0), 0.5 ng/mL (group R0.5), 1.0 ng/mL (group R1.0), and 1.5 ng/mL (group R1.5) during emergence. The emergence and recovery profiles were recorded. Adverse events such as coughing, airway obstruction, breath-holding, agitation, desaturation, nausea, and vomiting were also evaluated. RESULTS: The number of patients with respiratory complications such as coughing and breath-holding was significantly lower in the R1.0 and R1.5 groups than in the R0 group (p<0.05). Emergence agitation also decreased in the R1.0 and R1.5 groups (p<0.0083). The time to LMA removal was significantly longer in the R1.5 group than in the other groups (p<0.05). CONCLUSION: Maintaining a remifentanil Ce of 1.0 ng/mL during emergence may suppress adverse events such as coughing, breath-holding, and agitation following the removal of LMA without delayed awakening.

Conversion of supraventricular arrhythmia to normal rhythm by propofol and remifentanil: three cases report.

We experienced conversion of supraventricular arrhythmia to normal sinus rhythm in three patients during general anesthesia using propofol and remifentanil. This may be related to direct inhibition of the cardiac conduction system or activation of the parasympathetic system. The literature review suggests that propofol and remifentanil have antiarrhythmic potential, reverting supraventricular arrhythmia during anesthesia.

The comparison of feasibility and safety on fiberoptic guided intubation under conscious sedation with remifentanil and propofol.

BACKGROUND: Oropharyngeal manipulation is problematic when patients have a gag reflex. Sedation can suppress gag reflex, but can cause serious airway problems. We compared remifentanil (Group R) and propofol (Group P) in terms of cooperation and loss of gag reflex, while drugs were administered incrementally using target controlled infusion (TCI). METHODS: Fifty seven patients who required awake fiberoptic intubation were randomized to Group R or Group P. After measurement of baseline gag trigger point index (GTPI), TCI was set to effect-site concentration (Ce) of 1 ng/ml (Group R) or 1 µg/ml (Group P), then titrated by 0.5 increment until GTPI score reached 0. The incidence of drop-out and decreased cooperation, Ramsay sedation scale (RSS) and Ce at loss of GR, and complications were assessed. RESULTS: Seven patients were dropped out in Group P due to deep sedation and disobedient behavior, but none in Group R (P = 0.015). Gag reflex suppressed as RSS increased in both groups (P < 0.001), however, the incidence of elimination of gag reflex clustered at RSS 2 in Group R (P < 0.001), whereas it was evenly distributed in Group P (P = 0.20). The incidence of patients who were spontaneously roused (gag reflex elimination at RSS 1 and 2) were higher in Group R than in Group P (P = 0.002). CONCLUSIONS: Deep sedation and impaired cooperation were observed only in Group P and spontaneously roused patients were higher in Group R, suggesting that remifentanil is more suitable for cooperative elimination of GR.

Jaw-thrust induces sympathetic responses during induction of general anesthesia.

BACKGROUND: Jaw-thrust is a noxious stimulus that might induce sympathetic responses. The purpose of this study, was to evaluate the effects of jaw-thrust on sympathetic responses. METHODS: We investigated seventy three patients. Patients who received general anesthesia were randomly divided into a control group (maintenance of combined airway maneuver with head tilt, open mouth by mouthpiece, and chin-lift, n = 30) and jaw-thrust group (maintenance of head tilt, open mouth and jaw-thrust, n = 30). In the jaw-thrust group, four minutes of endoscopy-guided force to the mandible to get the best laryngeal view were applied. For the control group, the combined airway maneuver was maintained during the same period. Arterial blood pressure (AP) and heart rate (HR) were recorded at predetermined time points (1 min before anesthesia induction, 2 min after fiberoptic bronchoscopy placement, and thereafter 1 min-interval during each airway maneuver) during jaw-thrust and chin-lift maneuver. The force amplitude applied for best laryngeal view during jaw-thrust was also measured. RESULTS: Peak systolic and diastolic AP increased 39.0 ± 17.6 and 39.9 ± 22.8 mmHg from the baseline (P < 0.001) in the jaw-thrust group. HR was also 32.5 ± 19.4 beats/min from the baseline (P < 0.001) in the jaw-thrust group. These remained high at all time points, compared with the control group (P < 0.01). The force magnitude applied for jaw-thrust was not correlated to the AP and HR changes (P > 0.05). CONCLUSIONS: Performing the jaw-thrust maneuver induces significant sympathetic responses, irrespective of the force magnitude.

Extensive demyelinating change in cerebrum after a total knee replacement -A case report-.

Demyelination is characterized by the loss of myelin with the preservation of axons. Demyelinating diseases can be classified into several categories: demyelination due to inflammation, viral infection, osmotic derangements and hypoxic ischemia. In particular, osmotic myelinolysis is representative, and is associated with hyperosmolality, hypokalemia or rapid correction of hyponatremia. Osmotic myelinolysis was reported to be associated with underlying conditions, such as alcoholism, diuretics and malnutrition. A 67-year-old woman with hypertension was scheduled to undergo both total knee replacements (TKR). She was observed to be lethargic with dysphagia and quadriplegia after the second TKR. She had been taking diuretics for a long time, and did not have an adequate amount of food intake due to patient controlled analgesia and a gastric ulcer after the first TKR. A laboratory examination revealed hypokalemia but normonatremia. T2 weighted-MRI revealed abnormal high signal intensity in the basal ganglia and periventricular area. This case was diagnosed with osmotic myelinolysis associated with hypokalemia without an apparent sodium imbalance.

Misplaced central venous catheter in the jugular venous arch exposed during dissection before sternotomy.

Subclavian vein catheterization rarely results in misplacement of the central venous catheter (CVC) into the jugular venous arch (JVA). We present a case of misplacement of the CVC into the JVA during cardiac surgery.

Effects of propofol on early phase of warm hepatic ischemia/reperfusion injury.

BACKGROUND/AIMS: It is still unclear whether propofol may protect the liver against ischemia/ reperfusion injury (IRI) in vivo. METHODOLOGY: The livers of male Sprague-Dawley rats were subjected to 60 minutes of partial normothermic ischemia allowing perfusion to right and caudate lobes and subsequent 45 minutes of reperfusion. Either propofol (Propofol group, n = 11, 10 mg/ kg/h) or saline (Control group, n = 11) was continuously administered. At the end of reperfusion blood and liver samples were taken to analyze malondialdehyde, hepatic injury score, palmitate oxidation rate, serum AST and ALT concentrations. RESULTS: The malondialdehyde concentration (micromol/g tissue, mean +/- SD) was decreased in the Propofol group (1.39 +/- 0.21, perfused lobes and 1.85 +/- 0.27, ischemic reperfused lobes) compared with Control group (1.97 +/- 0.20, perfused lobes and 2.39 +/- 0.28, ischemic reperfused lobes) (P < 0.01). Hepatic injury scores were decreased in Propofol group compared with Control group (P < 0.01), but with mild hepatic injury in both groups. There were no differences of serum AST and ALT concentrations, and palmitate oxidation rate between groups. CONCLUSIONS: Propofol might be effective mainly in attenuation of lipid peroxidation with only minimal hepatocellular protection during the early phase of warm hepatic IRI in vivo.

Propofol attenuates Kupffer cell activation during hypoxia-reoxygenation.

PURPOSE: We undertook a study to determine whether propofol may attenuate Kupffer cell (KC) activation, thus protecting the cells against hypoxia-reoxygenation injury through the modulation of intracellular calcium ([Ca2+]i). METHODS: [Ca2+]i, the expression of tumour necrosis factor (TNF)-alpha mRNA, and KC viability were measured in response to hypoxia-reoxygenation following pretreatment with propofol 0.5 and 5 microg.mL(-1) (Groups P1 and P2, respectively) or without propofol (Group HRC). KCs were isolated and cultured from male Sprague-Dawley rats. KCs were incubated under an atmosphere of hypoxia (95% N2 + 5% CO2) for 60 min with subsequent 120 min reoxygenation (95% air + 5% CO2). [Ca2+]i for the first 12 min after reoxygenation, TNF-alpha mRNA, and KC viability at the end of reoxygenation in groups P1 and P2 were compared with those of HRC. RESULTS: The increase of [Ca2+]i from the baseline was attenuated in P1 (96.6 +/- 6.9%) and P2 (96.1 +/- 5.4%) compared with HRC (143.8 +/- 11.5%), (P < 0.001), with no difference between P1 and P2. The expression of TNF-alpha mRNA increased only in HRC during hypoxia-reoxygenation. KC viability increased in P1 (97.5 +/- 2.6%) and P2 (94.6 +/- 2.9%), compared with HRC (89.9 +/- 1.4%), (P < 0.005), with no difference between P1 and P2. CONCLUSION: The results indicate that propofol attenuates KC activation and protects KC from hypoxia-reoxygenation injury at clinically relevant concentrations. This attenuation seems to result from inhibition of [Ca2+]i increase in KC.

The effect of pudendal block on voiding after hemorrhoidectomy.

PURPOSE: Urinary retention in common benign anal surgery is a burden to ambulatory surgery. A pudendal nerve block was used in hemorrhoid surgery to reduce voiding complications. METHODS: The effects of a pudendal nerve block in anal surgery were compared with those of spinal anesthesia. In this prospective study, 163 consecutive patients who underwent elective hemorrhoids surgery by a single surgeon were randomized to receive pudendal nerve block (pudendal group) with 0.5 percent bupivacaine (n = 81) with 1:20,000 epinephrine or spinal anesthesia (spinal group) with 0.5 percentbupivacaine (n = 82). RESULTS: There were no statistically significant differences in the patient demographics, total amount of fluid administered, time to the onset of anesthesia, or intraoperative pain. All patients had a successful block during surgery. However, puborectalis muscle relaxation was not complete in the pudendal group. The time from the injection of the anesthetics to the first sensation of pain was longer in the pudendal group (9.1 vs. 3.1 hours; P < 0.001). Urinary catheterization was required in only 6 patients in the pudendal group compared with 57 patients in the spinal group (P < 0.001). The degree of pain was significantly lower in the pudendal group (2.7 vs. 5.2, Visual Analog Scale; P < 0.001). The amount of analgesics injected was significantly lower in the pudendal group (16/81 vs. 45/82; P < 0.001). CONCLUSIONS: A pudendal nerve block with bupivacaine results in fewer postoperative voiding complications and less pain compared with the traditional spinal anesthesia in a hemorrhoidectomy.

Gender may affect the hemodynamic response to induction and intubation in young adults.

STUDY OBJECTIVES: To determine whether gender affects the hemodynamic response to anesthesia induction and intubation in young adults. DESIGN: Randomized clinical trial. SETTING: University hospital. PATIENTS: 83 healthy patients, aged 20 to 30 years, scheduled for orthopedic, plastic, and general surgery. INTERVENTIONS: Patients were randomly allocated to one of three groups: Anesthesia was induced with fentanyl 1.5 microg/kg and thiopental 3 mg/kg in Group 1 (n = 28, men) and Group 2 (n = 28, women), or fentanyl 1.5 microg/kg and thiopental 2 mg/kg in Group 3 (n= 27, women) and maintained with enflurane 1% in N2O-O2 throughout the observational period. Three minutes after induction, direct laryngoscopy and intubation were performed. MEASUREMENTS: Noninvasive systolic (SBP) and diastolic (DBP) blood pressures, and heart rate (HR) were recorded before induction (baseline), immediately before intubation, immediately after intubation, and then every 1 minute for 5 minutes after intubation. RESULTS: SBP, DBP, and HR did not differ between men and women at baseline. However, SBP and DBP were lower in women than in men (p < 0.05) and immediately before intubation and at overall time points after intubation. There were no significant differences noted in SBP, DBP, and HR between Groups 2 and 3. When compared with baseline values, SBP and DBP were decreased in women, whereas only DBP was decreased in men immediately before intubation (p < 0.05). The increase in SBP was more prolonged in men after intubation. CONCLUSIONS: Pressor response is different in women than men, suggesting the difference of the response might result from the gender differences.

Lidocaine sprayed down the endotracheal tube attenuates the airway-circulatory reflexes by local anesthesia during emergence and extubation.

UNLABELLED: To determine whether lidocaine sprayed down the endotracheal tube (ETT) would attenuate airway-circulatory reflexes during emergence, we compared the reflex responses after endotracheal or IV lidocaine (IVL) in 75 patients receiving a standardized anesthetic protocol. At the end of surgery, the patients were divided into 3 groups (n = 25 for each group) and given no drug (Group 1), given 1 mg/kg of 2% lidocaine sprayed down the ETT 5 min before (Group 2), or given the same dose of IVL 3 min before extubation (Group 3). Blood pressure and heart rate were recorded at predetermined time points from 5 min (baseline) before until 5 min after extubation. The number of coughs per patient was continuously monitored during this period. The number (mean +/- SD) of coughs was decreased in Group 2 (4.5 +/- 3.7) compared with the control (10.2 +/- 6.0) (P < 0.01) with no difference for the control versus Group 3 (7.8 +/- 4.6). The increase in blood pressure was only attenuated immediately before extubation (P < 0.05), whereas the increase in heart rate was attenuated (P < 0.05) at all (except baseline) time points (P < 0.05) in Group 2 compared with the control with no difference for the control versus Group 3. The results indicate that lidocaine sprayed down the ETT suppresses the reflexes whereas using the same dose IVL does not, which is probably attributable to the mucosa-anesthetizing effect of lidocaine. IMPLICATIONS: Lidocaine sprayed down the endotracheal tube suppresses the airway-circulatory reflex responses whereas using the same dose IV lidocaine does not. This effect seems to be from the direct local anesthesia rather than from systemic absorption from the airway.