Michael Christopher Carey

The effects of intracuff lidocaine on endotracheal-tube-induced emergence phenomena after general anesthesia

UNLABELLED: Coughing during emergence from general anesthesia is a common clinical problem. We sought to determine whether inflating the endotracheal tube cuff with lidocaine would create a reservoir of local anesthetic, which might diffuse across the cuff membrane to anesthetize the mucosa, thus attenuating stimulation during extubation of the trachea. A total of 63 patients undergoing elective surgery were enrolled in a prospective, randomized, double-blinded study. After intubation of the trachea with an endotracheal tube, the cuff of the tube was inflated with either lidocaine 4%, saline, or air. After extubation, a blinded observer noted heart rate, blood pressure, oxygen saturation, end-tidal isoflurane concentration, and the incidence of coughing. Data were analyzed by using analysis of variance, Students t-test, and the chi(2) test for multiple variables. The groups were demographically comparable. There was no difference in hemodynamic or oxygen saturation data between either group. The incidence of coughing was decreased in the lidocaine group for the time period of 4-8 min postextubation (P < 0.05). We conclude that inflation of the cuff of the endotracheal tube can reduce the incidence of coughing in the initial postextubation period, a finding that may benefit certain patient groups in which this is particularly desirable. IMPLICATIONS: Tracheal intubation with an endotracheal tube is often necessary during anesthesia. After intubation, inflating a cuff around the endotracheal tube maintains a seal. This can result in coughing during emergence from anesthesia. Our study shows that inflating the cuff of an endotracheal tube with lidocaine rather than air can reduce the incidence of postextubation coughing.

Day-surgery patients anesthetized with propofol have less postoperative pain than those anesthetized with sevoflurane.

BACKGROUND: There have been recent studies suggesting that patients anesthetized with propofol have less postoperative pain compared with patients anesthetized with volatile anesthetics. METHODS: In this randomized, double-blind study, 80 patients undergoing day-case diagnostic laparoscopic gynecological surgery were either anesthetized with IV propofol or sevoflurane. The primary outcome measured was pain on a visual analog scale. RESULTS: Patients anesthetized with propofol had less pain compared with patients anesthetized with sevoflurane (P = 0.01). There was no difference in any of the other measured clinical outcomes. CONCLUSIONS: The patients anesthetized with propofol appeared to have less pain than patients anesthetized with sevoflurane.

Erythromycin accelerates gastric emptying in a dose-response manner in healthy subjects.

Study Objectives. To evaluate whether a dose‐response curve exists for erythromycin, determine the lowest effective dose of erythromycin needed to improve gastric motility, and compare erythromycins effectiveness with that of metoclopramide in improving gastric emptying.

Perioperative aspirin management after POISE-2: some answers, but questions remain.

Aspirin constitutes important uninterrupted lifelong therapy for many patients with cardiovascular (CV) disease or significant (CV) risk factors. However, whether aspirin should be continued or withheld in patients undergoing noncardiac surgery is a common clinical conundrum that balances the potential of aspirin for decreasing thrombotic risk with its possibility for increasing perioperative blood loss. In this focused review, we describe the role of aspirin in treating and preventing cardiovascular disease, summarize the most important literature on the perioperative use of aspirin (including the recently published PeriOperative ISchemic Evaluation [POISE]-2 trial), and offer current recommendations for managing aspirin during the perioperative period. POISE-2 suggests that aspirin administration during the perioperative period does not change the risk of a cardiovascular event and may result in increased bleeding. However, these findings are tempered by a number of methodological issues related to the study. On the basis of currently available literature, including POISE-2, aspirin should not be administered to patients undergoing surgery unless there is a definitive guideline-based primary or secondary prevention indication. Aside from closed-space procedures, intramedullary spine surgery, or possibly prostate surgery, moderate-risk patients taking lifelong aspirin for a guideline-based primary or secondary indication may warrant continuation of their aspirin throughout the perioperative period.

The Thrombotic and Arrhythmogenic Risks of Perioperative NSAIDs

From the *Department of Anesthesiology, University of New Mexico, Albuquerque, NM; †Department of Internal Medicine, Raymond G. Murphy VA Medical Center, Albuquerque, NM; and ‡Department of Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, OR. Address reprint requests to Neal Stuart Gerstein, MD, Department of Anesthesiology, MSC 10 6000, 2211 Lomas Blvd N.E. University of New Mexico, Albuquerque, NM 87120. E-mail: ngerstein@gmail.com

Oral albuterol to treat symptomatic bradycardia in acute spinal cord injury

Cardiovascular disturbances remain a leading cause of morbidity and mortality in patients with acute spinal cord injury (ASCI) [1]. This is particularly true for those with cervical and high thoracic spinal cord injuries. One series of 28,239 ASCI patients finds cardiac dysfunction responsible for 23 % of deaths within the first year of injury [2]. For patients with severe cervical spinal cord injury, persistent bradycardia is nearly universal and cardiac arrest is not uncommon [3]. The most common dysrhythmia, and the most worrisome, is symptomatic bradycardia because this rhythm disturbance often precedes cardiac arrest [1, 4]. Bradycardia affects as many as 35–71 % of patients with incomplete motor spinal cord injury [1]. These cardiovascular disturbances usually develop within 3–5 days following injury, and typically resolve in 6–8 weeks [5–7]. Although bradycardia associated with ASCI may resolve within 6–8 weeks after injury, medical management is important to prevent further symptomatic bradycardic episodes or cardiac arrest. The medical management options in this patient population are limited. Current medical management includes the use of methylxanthines (aminophylline and theophylline), dopamine infusions, or propantheline to avoid or to provide a safe bridge to pacemaker placement [6]. Atropine remains the drug of choice to treat an acute episode of bradycardia or cardiac arrest secondary to marked bradycardia [7]. Other medications that may be used to treat bradycardic episodes include epinephrine, pseudoephedrine and isoproterenol. Placement of a pacemaker is traditionally reserved for patients who are refractory to pharmacologic management, but Moerman et al. advocate for early pacemaker placement given the frequency of bradycardia and arrest in this patient population [8]. However, the natural history of ASCI-associated bradycardia is usually self-limited, and it may be possible to avoid pacemaker placement altogether if these individuals can be managed with medical treatment (Table 1). At our institution, a common practice has been to use oral albuterol elixir to treat patients with acute spinal cord injury and symptomatic bradycardia. When a patient is bradycardic during the initial resuscitation phase, it is our practice to use vasopressors or inotropic continuous infusions. Once a patient is considered to be resuscitated, if they remain bradycardic or develop symptomatic bradycardia that is believed to be secondary to their acute spinal cord injury, oral albuterol is started. The initial dose is usually 4 mg every 6 h. If this is found to be insufficient & Amber Rollstin arollstin@salud.unm.edu

There Is More to Postcraniotomy Emergence Hypertension Than Simply Blood Pressure Control-Why Nicardipine May Not Be the Drug of Choice.

To the Editor We read with great interest the article by Bebawy et al.1 concluding that nicardipine is superior to esmolol for the prevention of emergence hypertension. Although superior blood pressure control may be evident for nicardipine, blood pressure is perhaps not the most appropriate hemodynamic variable to predict the potential for postcraniotomy bleeding. Nicardipine may be inferior to esmolol for reducing bleeding and other adverse events. The study was underpowered to evaluate these endpoints. Esmolol is a β1-selective antagonist that decreases chronotropy and inotropy. Esmolol’s mechanism leads to decreases in left ventricular work and ejection velocity throughout systole. Nicardipine, a peripherally acting calcium channel blocker, decreases blood pressure by vasodilation. These hemodynamic principles are well recognized in the literature regarding the acute care of patients with aortic aneurysms.2,3 The initial treatment goal in the context of aneurysm pathology is to decrease the pulsatile load or the aortic wall stress (a function of change in pressure with time [dP/dT]) with β-blockade. In the acute setting, only after effective control of dP/dT should one initiate vasodilator therapy. The sole use of a vasodilator may decrease blood pressure, but without β-blockade, the pulsatile load will actually increase, potentially leading to adverse events including bleeding. The morbidity from emergence hypertension is primarily caused by bleeding. The likely mechanism is clot dislodgement after ineffective control of dP/dT. Hence, attenuating dP/dT should be the primary perioperative hemodynamic objective. Perhaps a more useful variable to measure would be cerebral blood flow. Cerebral blood flow will increase at emergence with the sympathetic surge and the release of endogenous catecholamines and is a good surrogate for 2. Ho AMH, Chui PT, Lee AP, Wan S. Hypertrophic cardiomyopathy apical variant. Cleve Clin J Med 2014;81:517–9 3. Parisi R, Mirabella F, Secco GG, Fattori R. Multimodality imaging in apical hypertrophic cardiomyopathy. World J Cardiol 2014;6:916–23 4. Kasirye Y, Manne JR, Epperla N, Bapani S, Garcia-Montilla R. Apical hypertrophic cardiomyopathy presenting as recurrent unexplained syncope. Clin Med Res 2012;10:26–31 5. Weir RA, MacKenzie N, Petrie CJ. Cheating the CHA2DS2VASc Score: thromboembolism in apical hypertrophic cardiomyopathy. Case Rep Cardiol 2014;2014:189895 6. Eriksson MJ, Sonnenberg B, Woo A, Rakowski P, Parker TG, Wigle ED, Rakowski H. Long-term outcome in patients with apical hypertrophic cardiomyopathy. J Am Coll Cardiol 2002;39:638–45