Elevating outcomes: Impact of 30° Head positioning on tracheal extubation in elective abdominal procedures

Ropivacaine is a long-acting amide local anaesthetic agent and first produced as a pure enantiomer. It produces effects similar to other local anaesthetics via reversible inhibition of sodium ion influx in nerve fibres. Ropivacaine is less lipophilic than bupivacaine and is less likely to penetrate large myelinated motor fibres, resulting in a relatively reduced motor blockade. Thus, ropivacaine has a greater degree of motor sensory differentiation, which could be useful when motor blockade is undesirable. The reduced lipophilicity is also associated with decreased potential for central nervous system toxicity and cardiotoxicity. The drug displays linear and dose proportional pharmacokinetics (up to 80 mg administered intravenously). It is metabolised extensively in the liver and excreted in urine. The present article details the clinical applications of ropivacaine and its current place as a local anaesthetic in the group.

This study aimed to investigate the trajectories of acute postoperative pain intensity during the initial 5days after abdominal surgery, and to analyze their association with the risk of developing chronic postsurgical pain (CPSP). We enrolled patients with elective abdominal surgery with pain measurements taken across postoperative days 1 through 5. Since postoperative pain is often unavoidable and its initial intensity is closely related to the invasiveness of the surgery, focusing on the overall pain trajectory may be more meaningful than evaluating pain at a single time point. Therefore, the primary outcome of this study was to identify distinct pain trajectories. Secondary outcome was the incidence of CPSP between differences pain trajectories. Lastly, mediation analyses were performed to explore the mediating role of the quality of recovery and subacute pain on the studied associations. The final analysis encompassed 1170 patients (36.75% female) with a median age of 55years. Two distinct clusters were identified: with movement (high: 533 [45.56%]; low: 637 [54.44%]) and at rest (high: 363 [31.03%]; low: 807 [68.97%]). Patients in the high pain trajectory group (during movement [odds ratio [OR] 2.04, 95% CI 1.56-2.68] or at rest [OR 1.90, 95% CI 1.44-2.53]) exhibited nearly doubled risk of CPSP. Moreover, these patients exhibited a significantly poorer recovery quality. Mediation analyses revealed that the poor recovery quality at postoperative 5days (17.62%-18.57%) and higher subacute pain at postoperative 1month (29.46%-32.75%) were significant mediators in the association between adverse postoperative acute pain trajectory patterns and CPSP. This study highlights the clinical significance of postoperative pain trajectory profiles in predicting the risk of CPSP, emphasizing postoperative acute pain trajectory as a critical indicator and subacute pain as a significant mediator. The findings underscore the potential for tailored pain management strategies targeting acute pain trajectories to reduce such risk.

What's New in Spine Surgery.

Background and Objectives: The gold standard for acute postoperative pain management in major abdominal surgeries is thoracic epidural analgesia (TEA) and this was proved by a lot of studies, systematic reviews and metaanalyses. However, TEA is sometimes contraindicated and may cause serious risks. Rectus Sheath Block (RSB) is effective for the abdominal surgeries with midline abdominal incisions as local anesthetics will be injected within the posterior rectus sheath bilaterally leading to intense pain relief for the middle anterior wall extending from the xiphoid process to the symphysis pubis. The aim of the study was to assess intra and post-operative RSB versus intra and post-operative TEA, in patients undergoing elective major abdominal cancer surgery with midline incisions. Methods: This randomized, blinded, was registered at www.clinicaltrials.gov at no.: “NCT03460561” and was approved by local ethics committee of South Egypt Cancer Institute, Assiut University, Egypt. One hundred adult patients, (ASA grade II and III), scheduled for major elective abdominal cancer surgery with Medline incision, were randomly divided into two groups, (50 patients each); TEA group: patients in this group received TEA with standard GA and intra-operative analgesia was started before skin incision by injecting epidural bolus dose of 0.1 ml/kg of (0.125% levo-bupivacaine+fentanyl 2 μg/ml). Postoperative analgesia was provided through PCEA by injecting a bolus dose of 3 ml then continuous infusion of 0.1 ml/kg of mixture of (0.0625% levo-bupivacaine+fentanyl 2 μg/ml) for 48 hours postoperative. RSB group: patients in this group received standard GA plus ultrasound (U/S) guided rectus sheath block by a volume of 20 mL of (0.25% levo-bupivacaine+fentanyl 30 μg) in saline on either side. Before end of surgery and before closure of abdominal wall, bilateral surgically placed catheters in rectus sheath plane aiming to provide post-operative analgesia using the following; 20 mL of (0.125% levo-bupivicaine+Fentanyl 30 μg) every 12 hours in to each catheter for 48 hours. Perioperative hemodynamics (MAP and HR) were recorded. Postoperative pain was assessed over 48 hour post operatively using (VAS). Total fentanyl consumption, Peak expiratory flow rate (PEFR), postoperative and side effects of the drugs and duration of ICU and hospital stay were recorded. Results: We found a significant reduction in VAS pain scores (at rest and during cough) in both group at all postoperative period but fentanyl consumption was significantly lower in TEA group. Also we found a significant reduction in intra-operative hemodynamics (mean arterial pressure and heart rate) in TEA group in comparison to RSB group while there was minimal statistically significant reduction in postoperative MAP and heart rate. The incidence of other postoperative complications such as sedation, nausea and vomiting were comparable in both groups. Conclusion: Rectus sheath block was not inferior to thoracic epidural analgesia in reduction of pain intensity after major abdominal cancer surgeries, and associated with hemodynamic stability along the 48 hours postoperative without procedure related adverse events or decreasing PEFR.

Recent studies suggest that intraperitoneal application of local anesthetics is useful in abdominal surgery. Tramadol and clonidine have specific effects on peripheral nerves when used alone. We aimed to evaluate the effects of intraperitoneal application of bupivacaine and the combinations of bupivacaine plus tramadol and bupivacaine plus clonidine on postoperative pain in total abdominal hysterectomy. After standard anesthetic procedure during closure of the abdomen, Group 1 (n = 20) was given 20 mL bupivacaine 0.5 percent, Group 2 (n = 20) was given 20 mL bupivacaine 0.5 percent plus 100 mg tramadol, and Group 3 (n = 20) was given 20 mL bupivacaine 0.5 percent plus 1 microg per kg clonidine, all into the peritoneal cavity. Postoperative pain was evaluated with the visual analog scale (VAS) at 30 minutes, and two, four, six, 12, and 24 hours after extubation. While patients were supine and seated, mean arterial pressure (MAP), heart rate (HR), and peripheral oxygen saturation (SpO2) values were noted. When VAS scores were 4 to 7, 0.5 mg per kg of meperidine was given intramuscularly (IM); above 7, 1 mg per kg of meperidine was given IM; and when VAS scores were 2 to 4, 500 mg acetaminophen was given orally. For evaluating quality of analgesia, rescue analgesic dose, analgesia time, and side effects were noted. The groups were similar in respect to SpO2; however, when Group 1 was compared to Groups 2 and 3 at 30 minutes, and two, four, and six hours, MAP and HR measurements were found to be significantly higher (p < 0.05). VAS values in sitting and supine positions at 30 minutes and two hours were significantly lower in Group 2 (p < 0.05) when compared to Group 1. VAS values for Group 3 at 30 minutes, and two and four hours in the supine position, and at 30 minutes and two hours in the sitting position, were found to be significantly lower than those in Group 1 (p < 0.05). There were no significant differences between Groups 2 and 3. The mean dosage of meperidine used was 76.7+/-10.5 mg in Group 1, 63.9+/-8.4 mg in Group 2, and 70 +/-5.2 mg in Group 3. When Group 1 was compared to Group 2, there were significant differences found (p < 0.05). First analgesic requirement time was found to be 30 (range, 30 to 30) minutes in Group 1, 120 (range, 30 to 240) minutes in Group 2, and 110 (range, 30 to 240) minutes in Group 3. There were significant differences found when Groups 2 and 3 were compared to Group 1 (p < 0.05). We concluded that the combinations of bupivacaine plus tramadol and bupivacaine plus clonidine administered intraperitoneally in total abdominal hysterectomy operations provide more effective analgesia than bupivacaine alone during the early postoperative period.

The purpose of this cardiac fast-track study was to evaluate the use of remifentanil (R) combined with intrathecal (IT) morphine as an alternative to sufentanil (S) during desflurane anesthesia with respect to postoperative pain control. Prior to entering the operating room, patients in the R group (n = 20) received morphine, 8 microg/kg IT. Anesthesia was induced using a standardized anesthetic technique in all patients. In the R group, anesthesia was maintained with R, 0.1 microg. kg(-1). min(-1) in combination with desflurane 3-10%. In the S group (n = 20), patients received S 0.3 microg. kg(-1). h(-1) and desflurane 3-10%. There were no differences between the two groups with respect to time from arrival in the intensive care unit to tracheal extubation (5.1 +/- 4.3 h vs 5.8 +/- 6.7 h for R and S groups, respectively). After extubation, patients in the R group had significantly lower visual analog pain scores, reduced patient-controlled analgesic requirements, and greater satisfaction with their perioperative pain management, compared with patients in the S group. We conclude that R combined with IT morphine provided superior pain control after cardiac surgery compared with a S-based general anesthetic technique. As part of a cardiac fast-tracking program involving desflurane anesthesia, the use of intrathecal morphine in combination with a remifentanil infusion provided improved postoperative pain control, compared with IV sufentanil alone.

To explore the effect of dexmedetomidine in acute postoperative pain and remifentanil-induced hyperalgesia. From January 2011 to June 2012, 120 patients scheduled for elective abdominal surgery under general anesthesia were included in this study. All patients received intravenous remifentanil infusion during operation, and dexmedetomidine was given after anesthesia induction. The postoperative mechanical pain threshold, pain visual analog scale (VAS) score, morphine consumption, and score of sedation (Ramsay) was recorded. Relatively large-dose intraoperative remifentanil resulted in lower mechanical pain threshold and higher dose of postoperative morphine consumption. Dexmedetomidine reduced postoperative morphine consumption significantly, and increased Ramsay scores, but had no effect on mechanical hyperalgesia. Dexmedetomidine can alleviate the acute postoperative pain effectively, but the effect is not dependent on inhibiting remifentanil-induced hyperalgesia.

Intraoperative Positioning of Patients Under General Anesthesia and the Risk of Postoperative Pain and Pressure Ulcers

To the Editor, In a randomized controlled trial in morbidly obese patients undergoing bariatric surgery, Wong et al. compared the Boussignac continuous positive airway pressure (CPAP) mask with a venturi mask and showed that the Boussignac CPAP mask can improve early postoperative oxygenation as measured by the PaO2/FIO2 ratio. These results make a valuable contribution to the treatment of postoperative respiratory insufficiency following bariatric surgery, which is a major concern for morbidly obese patients. However, in our view, there are two issues related to this study that warrant cautious interpretation of the results. First, the patient position during the early postoperative period is not clearly documented. Considering the potentially deleterious effects of supine positioning on pulmonary function in morbidly obese patients, these patients are more optimally managed in a non-supine position. During the first 48 postoperative hours after abdominal surgery, it has been shown that arterial oxygenation in morbidly obese patients is better maintained in the semi-recumbent position rather than in the supine position. Furthermore, morbidly obese patients placed in a reverse Trendelenburg position have improved pulmonary compliance and increased functional residual capacity, which improves oxygenation relative to the supine position. In our view, an important variable to consider is whether Wong et al. maintained identical positioning in all patients when evaluating the effects of the two respiratory treatments on postoperative pulmonary function. Second, although pain scores were reported to have been similar in the two groups at all time points, the article did not specify the postoperative analgesic protocol used in the two groups. This makes it difficult to assess whether all patients were ensured adequate postoperative analgesia. Following bariatric surgery, pain is recognized as being the most frequent postoperative problem, even for surgery that is performed laparoscopically. Inadequate postoperative analgesia results in splinting with rapid and shallow breathing. Furthermore, in morbidly obese patients, intensity of postoperative pain influences the extent of postoperative atelectasis 24 hr after tracheal extubation. Thus, ensuring optimal analgesia for morbidly obese patients in the postoperative period is of great importance, not only for patient comfort but also for improvement of pulmonary function and a reduction in the risk of respiratory complications. We recognize that providing optimal postoperative pain relief for morbidly obese patients remains a major challenge for modern anesthetic practice. For example, use of opioids is often inevitable to achieve satisfactory postoperative pain control, especially when regional anesthetic techniques are either difficult or impossible for anatomical reasons. Morbidly obese patients are at a very high risk for postoperative exacerbation of respiratory depression, with further depression with the administration of opioids. For this reason, standardization of the postoperative analgesic protocol should be an important element of the study design when evaluating effects of different treatments on He Ping Liu and Fu Shan Xue contributed equally to this work.

Children undergoing chemotherapy experience exacerbated postoperative pain and prolonged pain perception. Intraoperative intravenous administration of S-ketamine can alleviate postoperative pain. However, its efficacy in mitigating chemotherapy-induced hyperalgesia remains uncertain. This study evaluates the effect of S-ketamine on postoperative pain sensitivity in children who received preoperative chemotherapy. A total of 40 children undergoing preoperative chemotherapy and scheduled for open abdominal surgery were recruited from our center and randomly assigned to either the S-ketamine group or the control group. The primary outcomes included postoperative mechanical pain threshold, FLACC scale, Wong-Baker FACES pain rating scale (WBS), and cases of additional analgesic use. Secondary outcomes included intraoperative hemodynamic changes, extubation time, and incidence of adverse events. Thirty-six children were included in the study. The two groups had no significant difference in preoperative mechanical pain thresholds (P = 0.585). Patients receiving S-ketamine had higher mechanical pain thresholds at 24 and 48 h post-surgery (both P < 0.001). Preoperative FLACC and WBS were 0 in both groups. Postoperative FLACC and WBS showed significant differences at various time points (all P < 0.05). There is a negative correlation between infusion time of S-ketamine and postoperative mechanical pain threshold at 24 h (r = -0.570, P = 0.014) and 48 h postoperatively (r = -0.643, P = 0.004) in the S-ketmanie group. Intravenous S-ketamine significantly increases postoperative mechanical pain threshold and reduces pain in patients who received neoadjuvant chemotherapy. Children undergoing chemotherapy experience exacerbated postoperative pain and prolonged pain perception. Intraoperative intravenous administration of S-ketamine can alleviate postoperative pain. However, its efficacy in mitigating chemotherapy-induced hyperalgesia remains uncertain. This study fills the gap in this area. This study evaluates the effect of S-ketamine on postoperative pain sensitivity in children who received preoperative chemotherapy. S-ketamine's NMDAR antagonism may partly reduce pain sensitivity, thus reversing the pain effect. The results of this study provide promising evidence for the potential benefits of S-ketamine in improving postoperative pain outcomes in this patient population. The infusion time of S-ketamine ranged from 30 to 655 min, suggesting that the beneficial effect can be achieved within this time frame.

There is mounting evidence to suggest that immersive virtual reality (IVR) can improve pain in older adults in community settings, yet the use of IVR postoperatively in the acute postoperative period following major elective abdominal surgery remains largely underexplored. This single-arm pilot study aimed to assess the feasibility, acceptability, and preliminary impact of IVR on self-reported postoperative pain and relaxation levels in older adults following elective major abdominal surgery. We recruited individuals aged 55 years and older undergoing elective abdominal surgery at an academic medical center from October 2023 to February 2024. We evaluated feasibility through accrual rate, intervention completion, and questionnaire compliance; acceptability via the System Usability Scale (SUS) and a user experience survey; and tolerability by monitoring self-reported side effects. The preliminary impact of IVR on self-reported pain intensity and relaxation levels was assessed through pre- and postintervention comparisons. A total of 29 participants, with a median age of 73 (IQR 55-81) years, were enrolled and completed at least 1 IVR session, with 19 also completing a second session. Perceived usability and overall acceptance of IVR were high, with minimal side effects reported. In terms of the preliminary impact of IVR, statistically significant improvements were observed in both pain and relaxation levels from pre- to post-IVR on day 1 and day 2. This study suggests the feasibility and acceptability of IVR as a potential future intervention for postoperative pain management and enhancing relaxation among older adults following elective inpatient abdominal surgery. The preliminary findings suggest the need for large-scale studies across additional complex inpatient abdominal surgeries to confirm the acceptance and efficacy of IVR as a postoperative pain management intervention across a wide range of diverse older demographics. Future research is critical to evaluating the therapeutic potential of IVR in a variety of surgical and patient-specific contexts.

To evaluate the analgesic efficacy and safety of different does of intravenous ibuprofen (IVIB) in the treatment of postoperative acute pain. Patients with an intravenous (IV) patient-controlled analgesia device after abdominal or orthopedic surgery were randomly divided into placebo, IVIB 400 mg, and IVIB 800 mg groups. The first dosage of study medicines was given intravenously 30 minutes (min) before surgery ended, followed by six hours (h) intervals for a total of eight doses following surgery. The demographic characteristics and procedure data, cumulative morphine consumption, the visual analog scale (VAS), the area under the curve (AUC) of VAS, patient satisfaction score (PSS), the rates of treatment failure (RTF), and adverse events (AEs) and serious adverse event (SAEs) were recorded during the period of trial. A total of 345 patients were enrolled in the full analysis set (FAS), and of 326 participants were valid data set (VDS). Demographic characteristics, disease features, and medical history of patients were not significantly different between groups. Total morphine consumption of the IVIB 400 mg group (11.14 ± 7.14 mg; P = 0.0011) and the IVIB 800 mg group (11.29 ± 6.45 mg; P = 0.0014) was significantly reduced compared with the placebo group (14.51 ± 9.19 mg) for 24 h postoperatively, there was no significant difference between the IVIB 400 mg and IVIB 800 mg groups (P = 0.9997). The placebo group had significantly higher VAS and the AUCs of VAS than those in the IVIB 400 mg and the IVIB 800 mg groups at rest and movement for 24 h postoperatively (P < 0.05), and there was no significant difference between the IVIB 400 mg and IVIB 800 mg groups (P > 0.05). RTF was slightly higher in the placebo group than IVIB 400 mg group and 800 mg group, and no statistical significance (P < 0.690). PSS in the IVIB 400 mg (P = 0.0092) and the IVIB 800 mg groups (P = 0.0011) was higher than the placebo group for pain management, there was also no significant difference between the IVIB 400 mg and IVIB 800 mg groups (P = 0.456). The incidence of RTF (P = 0.690) and AEs (P > 0.05) were not different among the three groups. Intermittent IV administration of ibuprofen 400 mg or 800 mg within 24 h after surgery in patients undergoing abdominal and orthopedic surgery significantly decreased morphine consumption and relieved pain, without increasing the incidence of AEs.

This Month in Anesthesiology

Postoperative Tracheal Extubation

Although tracheal intubation receives much attention, especially with regard to management of the difficult airway, tracheal extubation has received relatively little emphasis. The scope and significance of problems occurring after tracheal extubation are real. Adverse outcomes involving the respiratory system comprise the single largest class of injury reported in the ASA Closed Claims Study [1]. Obvious adverse events related to tracheal extubation accounted for 35 of the 522 or 7% of the respiratory-related claims. Certainly additional morbidity related to extubation could be accounted for in other categories of adverse respiratory events, such as inadequate ventilation, airway obstruction, bronchospasm, and aspiration. Others have documented a 4%-9% incidence of serious adverse respiratory events in the immediate postextubation period [2,3] and preventable anesthesia-related etiologies were noted as important by Ruth et al. [2]. Mathew et al. [4], in a retrospective review of more than 13,000 anesthetics, noted that emergency tracheal reintubations occurred in only 0.19% of patients, and that the majority of tracheal reintubations were due to preventable anesthesia-related factors. Perhaps a greater percentage of patients experience postextubation difficulties but do not require reintubation of the trachea. Reasons for tracheal reintubation in the intensive care setting may differ, but the reported incidence in that arena is similarly 4% [5]. Anesthesiologists recognize the immediate postextubation period as one where patients are particularly vulnerable. Events such as laryngospasm, aspiration, inadequate airway patency, or inadequate ventilatory drive can occur and frequently result in hypoxemia. Such hypoxemia is most often corrected within minutes. Less frequently, postextubation hypoxemia can rapidly result in serious morbidity. In this report we will review the known physiologic and pathophysiologic changes associated with anesthesia and surgery that can influence respiratory function after tracheal extubation, the physiologic impact of extubation itself, criteria used for predicting successful extubation, and different techniques and interventions used for tracheal extubation. It is not our intent to review the complications of laryngoscopy and tracheal intubation. However, common complications of tracheal intubation, with special emphasis on the airway, will be discussed in detail as they frequently affect respiratory function after tracheal extubation. More uncommon and miscellaneous complications, such as problems related to the endotracheal tube cuff, recently have been reviewed [6]. Effects of Anesthesia and Surgery on Respiratory Function After Extubation After the "ideal" extubation, patients would exhibit adequate ventilatory drive, a normal breathing pattern, a patent airway with intact protective reflexes, normal pulmonary function, and the absence of any mechanical perturbations such as coughing. Unfortunately, all of these conditions are rarely, if ever, achieved in patients extubated after anesthesia. Understanding the potential interactions between anesthesia, surgery, and extubation on respiratory function helps define many of the complications that occur at this crucial juncture in anesthesia care. This section will include a discussion of the effects of anesthesia and surgery on the respiratory system which are common during extubation, with major emphasis on the airway and lung. Airway Changes Any form of airway dysfunction, such as obstruction after tracheal extubation, is an immediate threat to patient safety. Significant airway compromise leads to diminished minute ventilatory volumes and hypoxemia ensues in a variable, but often rapid fashion. A differential diagnosis of acute postoperative obstruction of the upper airway after extubation includes: laryngospasm, relaxed airway muscles, soft tissue edema, cervical hematoma, vocal-cord paralysis, and vocal-cord dysfunction Table 1. Airway obstruction from foreign body aspiration (e.g., temperature probe condoms) will not be reviewed but deserves mention.Table 1: Differential Diagnosis of Postoperative Airway ObstructionLaryngospasm Laryngospasm, defined by Keating [7] as a protective reflex, can be life-threatening when it occurs after extubation. Historically, a patient in Stage II anesthesia has been thought to be particularly vulnerable to laryngospasm [8]. Stimulation of a variety of sites from the nasal mucosa to the diaphragm can evoke laryngospasm [9]. Most commonly, laryngospasm is a reaction to a foreign body or substance near the glottis. Blood or saliva, even in small amounts, can elicit laryngospasm. It has been suggested that laryngospasm can be prevented by extubating a patient under deep anesthesia, while the laryngeal reflexes are depressed [8]. However, substantial proof of this tenet is lacking. Suzuki and Sasaki [10] contend that laryngospasm is solely attributable to prolonged adduction of the vocal cords mediated via the superior laryngeal nerve and cricothyroid muscle. Ikari and Sasaki [11] have demonstrated that the firing threshold of the laryngeal adductor neurons involved in laryngospasm varies in a sinusoidal manner during spontaneous ventilation. Interestingly, reflex laryngeal closure occurs more readily during expiration than inspiration Figure 1. Others believe that laryngospasm also involves closure of the glottis in addition to adduction of the vocal cords. Closure of the glottis results from contraction of the lateral cricoarytenoid and thyroarytenoid muscles, which are innervated by the recurrent laryngeal nerve [9]. Clinical recognition and treatment of laryngospasm must be expedient (see below), if complications such as hypoxemia or pulmonary edema are to be avoided [12].Figure 1: Mean threshold in volts for reflex glottic closure (laryngospasm) plotted with respect to respiratory phase. Note the increased threshold during inspiration. (Adapted with permission from: Ikari T, Saski CT. Glottic closure reflex control mechanisms. Ann Otol 1980;89:220-4.)Airway Relaxation Airway obstruction related to relaxation of airway soft tissue is frequently associated with residual effects of anesthesia. Such obstruction is purported to be most commonly due to relaxation of the airway (pharyngolaryngeal) muscles. Physiologic maintenance of upper airway patency occurs by a complex mechanism that involves the muscles inserted into the hyoid bone and thyroid cartilage [13]. During normal inspiration, an increase in tonic activity of these strap muscles precedes contraction of the diaphragm and prevents apposition of the tongue and soft palate against the posterior pharyngeal wall [14]. Drummond [15], administered sodium thiopental to 14 patients which resulted in a decrease in electromyographic activity of the strap muscles that was associated with airway obstruction. Airway collapse has been prevented by stimulation of the strap muscles in rabbits [16]. The mechanisms of airway obstruction in sleep disorders also involves a decrease in the tonic activity of these upper airway muscles. The actual tissue producing obstruction is a point of debate, but likely sites include the tongue, soft palate, and/or epiglottis. Evidence implicating the tongue as responsible for upper airway obstruction after extubation is derived from several sources including descriptions of the mechanism of obstruction in unconscious patients, other sleep apnea studies, and several anesthesia reports [17-21]. Safar et al. [17], after evaluating lateral radiographs in anesthetized patients concluded that obstruction is secondary to posterior prolapse of the tongue. Sleep apnea patients also experience obstruction from relaxation of the tongue secondary to decreased airway muscle tone that occurs during rapid eye movement sleep [18,19]. Studies using electromyograms in obstructive sleep apnea patients have recorded decreased activity of the genioglossus muscle concurrent with airway obstruction [19]. Nishino et al. [20], reported decreases in hypoglossal nerve activity which correlated inversely with increasing halothane concentrations in cats; however, there were no observations concerning airway obstruction. In addition, reports of intraoperative airway obstruction during bilateral carotid endarterectomy under cervical plexus block suggest bilateral hypoglossal nerve dysfunction as a contributing factor [21]. Using fluoroscopy and lateral radiography, others have demonstrated that obstruction occurs at the level of the soft palate in sleep apnea patients [22]. Nandi et al. [23] demonstrated obstruction at the soft palate in 17 of 18 patients, the epiglottis in 4 of 18 patients, and the tongue in 0 of 18 patients Figure 2 and Figure 3. Boiden [24], using bronchoscopy, had similar findings, and proposed that the relative position of the hyoid bone to the thyroid cartilage determines the degree of airway patency [24]. Thus, the head tilt and jaw thrust recommended by Morikawa et al. [25] results in ventral movement of the hyoid bone relative to the thyroid cartilage, and is effective in opening the airway. The soft palate appears to be the most likely site of airway obstruction. Nevertheless, prolapse of the tongue, especially when it is large, can probably also impair airway patency.Figure 2: Radiographic evidence before (left) and after (right) induction of anesthesia, demonstrating soft palate obstruction of the airway during anesthesia. Arrows indicate airway opening and narrowing. (Adapted with permission from Nandi PR. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991;66:157-62.)Figure 3: Diagrammatic representation of the pharyngeal outline based on radiograph Figure 2 measurements before (solid line) and after (dotted line) induction of anesthesia. 1, soft palate; 2, base of tongue; 3, hyoid bone; 4, epiglottis. (Adapted with permission from Nunn JF. Effect of general anaesthesia on the pharynx. Br J Anaesth 1991;66:157-62.)Pharyngolaryngeal Edema Uvular and/or soft palate edema is a potential cause of postextubation airway obstruction [26]. The pathophysiology of uvular edema is undetermined, but suggested possibilities include mechanical trauma and/or impeded venous drainage from airway devices including endotracheal tubes [27], oral airways [28], nasal airways [29], laryngeal mask airways [30], and vigorous suctioning of the airway [31]. Pregnant patients, and especially those with toxemia, may experience significant uvular and/or pharyngolaryngeal edema and related airway obstruction [32]. Surgery involving the anterior neck, including dissections or cervical spine operations, may also result in pharyngolaryngeal edema and airway obstruction. Avoiding bilateral neck dissections in an attempt to prevent serious edema has been recommended [33], but, significant edema and supraglottic obstruction can occur even after delayed contralateral second stage procedures [34]. One proposed mechanism of edema after neck surgery is the physical disruption of lymphatic drainage. Emery et al. [35] presented a review of seven cases of postoperative upper airway obstruction after anterior cervical spine surgery. Five of the seven patients had evidence of pharyngolaryngeal edema, while none of the seven cases had evidence of cervical hematoma. Cervical Hematoma Cervical hematoma after anterior neck surgery can also cause airway obstruction. Such hematomas can develop postoperatively, and cause delayed airway obstruction after extubation. The purported mechanism of airway obstruction associated with cervical hematoma is the obstruction of venous and lymphatic systems by the expanding mass, resulting in pharyngolaryngeal edema [36]. Edematous mucosal folds can eventually obliterate the glottis [36]. Compression of adjacent airway structures, such as the trachea, by a hematoma is not commonly found [37]. O'Sullivan et al. [36], described the postoperative course of six carotid endarterectomy patients who formed cervical hematomas. Stridor and respiratory compromise, which required immediate surgical intervention, developed in four of six patients. After induction of general anesthesia, three of these patients were impossible to manually ventilate and two could not be intubated. The two patients without evidence of stridor also returned to the operating room. One of these two could not be manually ventilated and both were difficult to intubate. Another reported case of cervical hematoma involved a 57-yr-old patient who developed airway obstruction 12 h after thyroidectomy. A significant hematoma developed, but its evacuation did not relieve airway obstruction. The persistent airway obstruction was thought to be secondary to pharyngolaryngeal edema [38]. The incidence of cervical wound hematoma after carotid endarterectomy is cited as 1.9%, with an unknown percentage of these patients developing airway obstruction [39]. When these patients return to the operating room for reexploration, the absence of stridor or respiratory distress does not predict freedom from "difficult airway" problems. Hematoma, as well as pharyngolaryngeal edema, may render manual ventilation by mask and/or visualization of the vocal cords and tracheal intubation difficult or impossible. In addition, evacuation of the hematoma may not ameliorate existing airway compromise. Such patients should be extubated cautiously and when there is evidence that pharyngolaryngeal edema has diminished. Lingual Edema Oral surgery can produce edema of the tongue and compromise postoperative airway function, especially after palatoplasty or pharyngeal flap surgery [40]. Prolonged placement of a mouth gag, commonly used in cleft palate repair, can result in lingual edema as described by Schettler [41]. Periodic relief of pressure from mouth gag devices should help reduce associated lingual edema [42]. Head position during neurosurgery has also been reported to contribute to lingual edema. Patients undergoing a craniotomy in the sitting position may have their head in such extreme flexion that obstruction of venous drainage of the tongue results in lingual edema, macroglossia, and airway obstruction [43]. During such head flexion the presence of an oral airway may exacerbate compression of the tongue and further compromise lingual circulation. An allergic reaction to glutaraldehyde solution, used to sterilize laryngoscope blades, is another unique cause of lingual edema. Edema can be so severe as to lead to reintubation during recovery [44]. Severe allergic reactions in general may involve part or all of several airway structures and can also result in edema and airway compromise. Vocal Cord Paralysis Unilateral vocal cord paralysis may cause persistent hoarseness after extubation [45]. Bilateral vocal cord paralysis may produce upper airway obstruction [46,47]. Vocal cord paralysis is usually secondary to injury of the recurrent laryngeal nerve resulting in unopposed superior laryngeal nerve mediated adduction of the vocal cords. Such an injury can occur with neck surgery (especially thyroidectomy) [48], thoracic surgery [49,50], internal jugular line placement [51], and endotracheal intubation [52-55]. Endotracheal tubes are frequently cited as a cause of vocal cord paralysis, and suggested mechanisms include endotracheal tube cuff compression of the recurrent laryngeal nerve against the lamina of the thyroid cartilage. Positioning of the endotracheal tube cuff just below or adjacent to the vocal cords may increase the incidence of this problem. Excessive cuff inflation and/or high cuff pressures resulting from diffusion of nitrous oxide can also contribute to vocal cord damage, especially in cuffs that are positioned just below the cords. Vocal Cord Dysfunction Vocal cord dysfunction (VCD) is an uncommon clinical cause of airway obstruction. VCD was first described in 1902 by Osler [56]. It has since been described by various synonyms, including paroxysmal vocal cord motion [57], factitious asthma [58], emotional laryngeal wheezing [59], and Munchausen's stridor [60]. All of the above entities are similar in their clinical presentation. The patient population, from the few reported cases [61,62], appears to consist predominantly of young females with a recent history of an upper respiratory tract infection and emotional stress [59,61,63]. VCD presents with laryngeal stridor or upper airway wheezing similar to asthma [59,64], but the wheezing is unresponsive to bronchodilator therapy [58,63,65]. Patients complain of inspiratory difficulties that result from paradoxical adduction of the vocal cords during inspiration [59]. Obstruction can be severe and require the institution of an artificial or surgical airway [61,66]. Flow volume loops will reveal variable extrathoracic obstruction with a marked decrease in inspiratory flow compared to expiratory flow [61], but visualization of the vocal cords during a symptomatic episode is necessary for a definitive diagnosis [67]. Recommendations for successful extubation of these patients include avoiding an awake extubation or, if possible, providing adequate sedation at the time of extubation. Sedation alleviates the dynamic inspiratory obstruction by reducing inspiratory effort and flow. Treatment of a VCD episode includes verbal reassurance, asking the patient to focus on the expiratory phase of breathing [62], and sedation if the diagnosis of VCD as the cause of respiratory distress is certain [58]. Laryngeal Incompetence Several investigations have demonstrated that laryngeal incompetence occurs after extubation whether or not residual anesthetic effects are present. Tomlin et al. [68] evaluated 56 patients undergoing simple surface surgery under "light" balanced anesthesia; 12 patients developed postoperative atelectasis, 6 of whom aspirated when asked to swallow 10 mL of contrast medium 2 or more hours after surgery. The majority of these patients (4 of 6) demonstrating this finding had been intubated. Gardner [69] demonstrated aspiration in 10 of 94 patients 2 to 4 days after extubation, and Siedlecki et al. [70] found that 27% of responsive patients aspirated radiopaque dye immediately after extubation. Cardiac surgery patients also have a high risk (33%) of aspiration when extubated early (less than 8 h) after surgery, even if awake. This risk significantly decreases to 5% when extubation is performed later [71]. Residual anesthetic effects may contribute to this high incidence of aspiration in the early postoperative period. In summary, laryngeal incompetence is common and the risk of aspiration after extubation is not eliminated by the presence of consciousness. Swallowing Swallowing, another airway protection reflex, can also be impaired by a host of factors after surgery and anesthesia. As recently reviewed [72], topical anesthetics, tracheostomy, tracheal intubation, neurologic or airway structure injury, conscious intravenous sedation, inhalation of 50% nitrous oxide, and even sleep can depress swallowing and permit pulmonary aspiration. Pavlin et al. [73] and Isono et al. [74] have also demonstrated that partial paralysis with neuromuscular blockers depresses swallowing, too. Control of Breathing While it is not the purpose of this review to completely describe the impact of anesthesia on the control of breathing, it is necessary to highlight the major factors affecting ventilatory drive during tracheal extubation. Airway function is also linked to the central neural control of breathing and, like spontaneous ventilation, is depressed by anesthesia. Inhalation drugs, opioids, sedative-hypnotics, and muscle relaxants are the common anesthetics that can depress the ventilatory response to carbon dioxide and/or hypoxia. Significant residual drug effects are often present at the time of tracheal extubation. Inhalation drugs alter the regulation of CO2 partial pressures, as evidenced by the correlation between increasing alveolar concentrations of various potent inhaled anesthetics, and increases in resting CO2 tensions and declines in ventilatory responses to CO2[75-77]. Low concentrations of the potent inhalation drugs (less than 0.5 minimum alveolar anesthetic concentration (MAC)) should not, in and of themselves, produce clinically troublesome blunting of ventilatory response to CO2 during extubation and recovery from surgery [78]. However, low concentrations of potent inhalation drugs may blunt the hypoxic ventilatory response and such an effect can pose a significant risk. Halothane, enflurane, and isoflurane, at 1 MAC in dogs, produce significant depression of hypoxic ventilatory drive. Enflurane has been reported to be the greatest depressant of hypoxic ventilatory drive and isoflurane the least [79]. Knill et al. [78,80,81] performed several investigations of hypoxic ventilatory drives in humans and demonstrated that even low concentrations (0.1 MAC) of halothane and enflurane greatly decrease the ventilatory response to isocapnic hypoxia. A more recent report suggests that hypoxic ventilatory drive may not be depressed by low concentrations of isoflurane [82]. Decreases in hypoxic, but not hypercapnic, ventilatory drive occur with nitrous oxide as well [83]. All mu receptor opioid including and produce depression of ventilation, a on the respiratory The of the respiratory to CO2 is significantly by The of the ventilatory response to CO2 is and minute ventilatory responses to increases in are to the The threshold and resting are also increased by Thus, the mechanism the body minute ventilation and from significant increases in CO2 and respiratory is significantly impaired by also decrease hypoxic ventilatory drive and blunt the increase in respiratory drive associated with increased such as increased airway or recurrent respiratory depression can occur in patients from general anesthesia who have received and for this include a of stimulation or of and other after activity of in and have noted second in during the phase in produce decreases in CO2 and breathing have also been to decrease the acute ventilatory response to and This is not as as that after opioid of significant residual effects with can be by of the of of the and can also decrease hypoxic ventilatory drive, by in the carotid body is one of the carotid body involved in hypoxic ventilatory drive of troublesome ventilatory depression can occur after extubation without extubation, patient and recovery room can result in significant patient these events have stimulation can and result in an with inadequate and/or ventilation. especially in with the of opioid results in significant depression of ventilatory drive Function The significant physiologic and, at pathophysiologic changes during general anesthesia that can after tracheal extubation. changes frequently include decreased in of breathing, and depressed changes are rarely, if ever, of can be and, at may result in significant patient morbidity. Thus, the impact of anesthesia and surgery on function can significantly influence results after tracheal extubation. The most and volume after extubation is an increase in which occurs as a result of the endotracheal tube volume with the upper airway Significant changes in residual also occur usually decreases by of or mL with induction of general anesthesia Postoperative decreases in are associated with surgery of the or It is whether is decreased immediately after tracheal extubation. et al. and and demonstrated is not decreased immediately after extubation, it is decreased several hours et al. demonstrated a decrease in in of patients 1 h after surgery. The decrease in after induction of anesthesia and after extubation may be by different mechanisms The decrease in immediately after induction was well by et al. In that of compression Figure The mechanism for this decrease in after induction of anesthesia has been to a of the diaphragm and increased volume Interestingly, neuromuscular block after induction of general anesthesia does not result in a further decrease in The mechanism postoperative decreases in is usually related to dysfunction et al. reported that dysfunction after surgery could to 1 and resulted in a greater on movement for dysfunction is to be secondary to surgical inadequate and/or In addition to dysfunction, another cause of postoperative decreases in is breathing of can and and of the before and after induction of anesthesia, demonstrating of compression in the of both (Adapted with permission from et al. during anesthesia with of the clinical of decreases in are often not decreases in are often to cause Figure 4 and that impair and decrease Such volume if present at the time of extubation, can compromise a to airway difficulties by the time for and of hypoxemia. The incidence of most frequently defined as an than after extubation and recovery from general anesthesia is As many as of and of after a general anesthetic will be at a care if no is during and in a review of hypoxemia during and after anesthesia, postoperative into early and inadequate minute ventilation or airway obstruction, other of early hypoxemia include increased increased diffusion of hypoxic pulmonary and a decrease in include increased pulmonary hypoxemia more frequently than and Although the intraoperative of has been reported to increase postoperative hypoxemia the majority of have not demonstrated that the of in anesthesia is associated with an increased incidence of postoperative hypoxemia another cause of hypoxemia in patients from anesthesia was first reported by who thought the diffusion of could alveolar the of during and recovery from anesthesia the incidence of clinically significant diffusion is but not of dysfunction associated with anesthesia and surgery can also contribute to postoperative hypoxemia. from the respiratory tract Patients with have been to have delayed tracheal intubation and surgery result in dysfunction and or flow. in can contribute to impaired of Breathing extubation of a breathing patient can