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• W2108292671 abstract "Central neuraxial block is associated with increased vagal tone. We report a patient who developed laryngospasm and stridor under spinal anaesthesia. This was treated successfully with i.v. atropine and fluids. We propose that the laryngospasm was secondary to increased vagal tone under the spinal anaesthetic. Such a manifestation of increased vagal tone under spinal anaesthesia has not been reported previously. Central neuraxial block is associated with increased vagal tone. We report a patient who developed laryngospasm and stridor under spinal anaesthesia. This was treated successfully with i.v. atropine and fluids. We propose that the laryngospasm was secondary to increased vagal tone under the spinal anaesthetic. Such a manifestation of increased vagal tone under spinal anaesthesia has not been reported previously. Central neuraxial block is associated with increased vagal tone; the signs and symptoms vary from a benign bradycardia or nausea to a full blown cardiac arrest. We report a patient, who developed laryngospasm and stridor under spinal anaesthesia. We propose that the laryngospasm was secondary to increased vagal tone. Such a manifestation of increased vagal tone under spinal anaesthesia has not been reported previously. A 42-yr-old male, 170 cm tall, weighing 60 kg, was scheduled for elective debridement and split thickness skin grafting of both feet. He had been in a road traffic accident three months earlier and had undergone debridement under general anaesthesia, which was uneventful. He was known to have hypertension for the past 2 yr that was treated with bisoprolol 2.5 mg once a day. Before surgery, his blood pressure was well-controlled (130/80 mm Hg) and his pulse rate was 84 beats min−1. There was no evidence of end-organ damage. The electrocardiogram (ECG) did not show any evidence of ischaemic heart disease or left ventricular hypertrophy. Echocardiogram showed normal left ventricular function. He gave no history of gastro-oesophageal reflux. He tested positive for hepatitis B surface antigen, but there was no evidence of chronic active hepatitis or other known co-existing illnesses. Subarachnoid block was planned and the procedure was explained to the patient. He was kept fasting from midnight (solids) and was allowed water up to 7 a.m. on the day of surgery. The surgery was unexpectedly delayed by 3 h. The premedication, 1 h before the anaesthetic, consisted of diazepam 10 mg, metoclopramide 10 mg and his scheduled dose of bisoprolol. He had not taken the water that was allowed before 7 a.m. and hence had been fasting for approximately 14 h. In the operating theatre, a peripheral i.v. cannula was placed on the right fore-arm and infusion of sodium chloride 0.9% solution was started. The monitoring consisted of ECG, non-invasive blood pressure (NIBP) and pulse oximetry; the blood pressure was 120/74 mm Hg, heart rate 92 beats min−1 and oxygen saturation ( SpO2) 98% while breathing room air. He appeared anxious and midazolam 2 mg was administered i.v. in 0.5 mg increments over 5 min. Our aim was to achieve a sensory block level of T10 to cover the thigh (donor area). The expected duration of surgery was 2–2.5 h. The patient was turned to right lateral position and under strict aseptic precautions the skin and subcutaneous tissue were infiltrated with 2.5 ml lidocaine 2%. Lumbar puncture was performed in the L2–L3 interspinous space on the third attempt using a 25 gauge needle. The patient did not have any pain and/or paraesthesia during lumbar puncture. After establishing a clear flow of cerebrospinal fluid, hyperbaric bupivacaine 0.5% (12.5 mg), 2.5 ml was administered into the lumbar subarachnoid space. The patient was then turned supine. Five minutes later, his heart rate was 105 beats min−1, blood pressure 115/70 mm Hg and SpO2 98% while breathing room air. At this point of time there was a sensory block up to the level of T11. The surgeons were allowed to remove the dressing; the patient did not complain of pain. He was adequately sedated and arousable. A preload of sodium chloride 0.9%, 500 ml was planned, but only 100 ml had been infused owing to poor flow in the right lateral position during the lumbar puncture, which went unnoticed. Supplementary oxygen was not administered as the SpO2 on room air was 98%. Approximately 8 min after performing the subarachnoid block, the patient suddenly developed stridor and bradycardia (50 beats min−1). SpO2 dropped to as low as 60%; this may not have been the true value of SpO2 as there were artifacts caused by patient movement. The patient was awake and was indicating to us that he was not able to breathe. The surgeons were requested to stop removing the dressing; supplementary oxygen was administered via a closed breathing circuit and preparations were made for endotracheal intubation. The heart rate was 48 beats min−1, the blood pressure 70/30 mm Hg and the patient still awake. We planned to sedate him before proceeding to endotracheal intubation. Ketamine would have been the drug of choice; suxinylcholine in a low dose would break the laryngospasm and facilitate endotracheal intubation but could worsen bradycardia. Considering these factors, i.v. atropine 0.6 mg was administered to treat the bradycardia and i.v. infusion of fluids was rushed, followed by 12 mg of ephedrine i.v. to treat hypotension. There was a prompt reversal of the laryngospasm in the next 10–15 s and the patient exclaimed ‘Oh that was a different world’! His voice was normal. His heart rate had increased to 115 beats min−1, blood pressure to 124/65 mm Hg and the SpO2 was 100% while breathing oxygen. No sedation or neuromuscular blocking agent was used and the planned endotracheal intubation was abandoned. On subsequent examination, the sensory block to sharp pain was confirmed at the level of T9. The surgeons were allowed to proceed with the surgery as planned. The patient did not have any further problems. Postoperative period was uneventful and the patient was discharged from hospital on the fifth postoperative day. Increased vagal tone under central neuraxial block is a well-known phenomenon. It is more common during subarachnoid block than epidural block. The common manifestations of increased vagal tone are bradycardia, hypotension and nausea. Rarely, bronchospasm,1Wang CY Ong GS Severe bronchospasm during epidural anaesthesia.Anaesthesia. 1993; 48: 514-515Crossref PubMed Scopus (21) Google Scholar coronary artery spasm2Wahl A Elberli FR Thomson DA Luginbuhl M Coronary artery spasm and non-Q-wave myocardial infarction following intravenous ephedrine in two healthy women under spinal anaesthesia.Br J Anaesth. 2002; 89: 519-523Abstract Full Text PDF PubMed Scopus (24) Google Scholar3Imamura M Matsukawa T Kashimoto S Nonaka A Kumazawa T A case of coronary artery spasm during spinal anesthesia.J Clin Anesth. 1996; 8: 522-524Abstract Full Text PDF PubMed Scopus (12) Google Scholar and cardiac arrest4Auroy Y Narchi P Messiah A et al.Serious complications related to regional anaesthesia.Anesthesiology. 1997; 87: 479-486Crossref PubMed Scopus (931) Google Scholar have been reported. Thus vagotonia after subarachnoid block can present in various forms. Vagal stimulation is employed in treatment of intractable epilepsy. Stimulation of vagus is known to cause various reactions from subtle voice changes to cardiac asystole. The voice change is a result of change in vocal cord function. Different levels of vagal stimulation in these patients have shown various degrees of vocal cord dysfunction including abduction, adduction and laryngeal hemispasm.5Kersing W Dejonckere PH van der Aa HE Buschman HP Laryngeal and vocal changes during vagus nerve stimulation in epileptic patients.J Voice. 2002; 16: 251-257Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar6Lundy DS Casiano RR Landy HJ Gallo J Gallo B Ramsey RE Effects of vagal nerve stimulation on laryngeal function.J Voice. 1993; 7: 359-364Abstract Full Text PDF PubMed Scopus (43) Google Scholar Therefore, it is possible that the increased vagal tone associated with central neuraxial block can lead to vocal cord dysfunction; although this has not been reported before. Laryngospasm and stridor are common in patients under general anaesthesia. Painful stimulus, peritoneal traction and laryngeal irritation under inadequate depth of anaesthesia all can precipitate laryngospasm. It can also occur in conscious patients in the presence of bilateral abductor paralysis associated with incomplete recurrent laryngeal nerve injury, in the presence of residual neuromuscular block, any cause of narrowing of the glottis like laryngeal neoplasm, laryngeal oedema after instrumentation of the larynx and angioedema. Stridor is associated with paradoxical vocal cord motion (PVCM)7Maschka DA Bauman NM McCray Jr, PB Hoffman HT Karnell MP Smith RJ A classification scheme for paradoxical vocal cord motion.Laryngoscope. 1997; 107: 1429-1435Crossref PubMed Scopus (116) Google Scholar and has been described in patients in the recovery room after surgery.8Arndt GA Voth BR Paradoxical vocal cord motion in the recovery room: a masquerader of pulmonary dysfunction.Can J Anaesth. 1996; 43: 1249-1251Crossref PubMed Scopus (24) Google Scholar9Larsen B Caruso LJ Villariet DB Paradoxical vocal cord motion: an often misdiagnosed cause of postoperative stridor.J Clin Anesth. 2004; 16: 230-234Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar PVCM is associated with psychogenic stridor that can be seen in anxiety states and conversion reactions in psychiatric patients. After subarachnoid block, reductions of the right atrial pressures by 36% to 54% have been reported.10Sancetta SM Lynn RB Simeone FA Scott RW Studies of hemodynamic changes in humans following induction of low and high spinal anesthesia.Circulation. 1952; 6: 559-571Crossref PubMed Google Scholar11Lynn R Sancetta S Simeone F Scott R Observations on the circulation in high spinal anesthesia.Surgery. 1952; 32: 195-213PubMed Google Scholar The right atrial pressures can drop by 66% with an associated blood loss equivalent of 10% of body weight.12Kennedy Jr, WF Bonica JJ Akamatsu TJ et al.Cardiovascular and respiratory effects of subarachnoid block in the presence of acute blood loss.Anesthesiology. 1968; 29: 29-35Crossref PubMed Scopus (30) Google Scholar Baron and colleagues13Baron JF Decaux-Jacolot A Edourd A et al.Influence of venous return on baroreflex control of heart rate during lumbar epidural anesthesia in humans.Anesthesiology. 1986; 64: 188-193Crossref PubMed Scopus (92) Google Scholar have shown that the reduction in venous return is primarily responsible for the increase in vagal tone. Jacobsen and colleagues14Jacobsen J Sofelt S Brocks V et al.Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia.Acta Anaesthesiol Scand. 1992; 36: 831-836Crossref PubMed Scopus (48) Google Scholar have demonstrated that the increased vagal tone was reversed with restoration of filling by rapid fluid infusion and head down position. Also it has been shown in experimental settings that the response to reduced venous return may be more than just bradycardia, and it may include sweating, nausea, syncope15Murray RH Thompson LJ Bowers JA Albright CD Hemodynamic effects of graded hypovolemia and vasodepressor syncope induced by lower body negative pressure.Am Heart J. 1968; 76: 799-811Abstract Full Text PDF PubMed Scopus (132) Google Scholar and cardiac arrest.15Murray RH Thompson LJ Bowers JA Albright CD Hemodynamic effects of graded hypovolemia and vasodepressor syncope induced by lower body negative pressure.Am Heart J. 1968; 76: 799-811Abstract Full Text PDF PubMed Scopus (132) Google Scholar16Bonica JJ Kennedy WF Akamatsu TJ Gerbershagen HU Circulatory effects of peridural block: 3. Effects of acute blood loss.Anesthesiology. 1972; 36: 219-227Crossref PubMed Scopus (46) Google Scholar Reviewing the literature on patients who developed bradycardia and cardiac arrest during subarachnoid block, Pollard17Pollard JB Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention.Anesth Analg. 2001; 92: 252-256Crossref PubMed Scopus (121) Google Scholar has described risk factors for vagal predominance. These are baseline heart rate <60, ASA physical status I (vs III or IV), use of β-blocking drugs, sensory block at level above T6, age <50 yr and prolonged PR interval. Our patient had at least two of these risk factors; namely age <50 yr and β-blocker therapy. Subsequently, Pollard18Pollard JB High doses of local anaesthetic during spinal anaesthesia may increase the risk of life-threatening vagal reactions.Br J Anaesth. 2003; 90: 525-526Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar has reviewed the risk of life-threatening vagal reactions when high dose of local anaesthetic is used in spinal anaesthesia in response to the case report of Wahl and colleagues.2Wahl A Elberli FR Thomson DA Luginbuhl M Coronary artery spasm and non-Q-wave myocardial infarction following intravenous ephedrine in two healthy women under spinal anaesthesia.Br J Anaesth. 2002; 89: 519-523Abstract Full Text PDF PubMed Scopus (24) Google Scholar Furlan19Furlan JC Sympathetic fiber origin of the superior laryngeal nerve and its branches: an anatomic study.Clin Anat. 2002; 15: 271-275Crossref PubMed Scopus (13) Google Scholar has demonstrated interconnections between the sympathetic chain, superior cervical ganglion and the superior laryngeal nerve in human larynx. Though the physiological significance of sympathetic innervation to the laryngeal motor function is not known, a fine balance of the sympathetic and parasympathetic signals for the normal functioning of the vocal cords could exist. The sympathetic block associated with high levels of central neuraxial block may disturb this balance resulting in functional vocal cord movement disorder resulting in stridor. We put forth the following reasons to substantiate our case in favour of increased vagal tone as the aetiology of laryngospasm. Our patient though appeared calm, was anxious. He was sedated with a small dose of midazolam and was arousable. Though midazolam is known to precipitate stridor,20Davis DP Hamilton RS Webster TH Reversal of midazolam-induced laryngospasm with flumazenil.Ann Emerg Med. 1998; 32: 263-265Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar given the sequence of events it is an unlikely aetiology in our case. We did not administer anxiolytics or sedatives subsequently and the patient did not have further recurrence of the symptoms intraoperatively or postoperatively; a psychological aetiology for the laryngospasm is therefore unlikely. Dystonic reactions are known to be caused by dopamine antagonists like metoclopramide. Our patient did not have any other manifestation of dystonic reaction like extrapyramidal signs, muscle stiffness or torticollis. Hence laryngeal dystonia secondary to metoclopramide administered with the premedication is an improbable aetiology. He did not have any history of gastro-oesophageal reflux nor had any gastric contents in his mouth when he developed the stridor. He was not subjected to any painful stimulus as the surgeons were allowed to remove the wound dressing only after ensuring adequate sensory block. He did not develop anaphylaxis or angioedema. He did not suffer from any psychiatric illness nor had similar episodes pre- or postoperatively. Increased vagal tone was a result of the subarachnoid block in our patient who probably had pre-existing intravascular volume deficit. The volume deficit could have been a result of multiple factors such as prolonged fasting, hot climate during the summer in South India and almost no preloading before the subarachnoid block. The only indication of fluid deficit before the block was sinus tachycardia (92 beats min−1) despite β-blocker therapy. At the time this was thought to be secondary to patient anxiety. Laryngospasm was associated with bradycardia and hypotension and was promptly relieved by vagolysis with atropine and fluid loading. Fluid loading of 750 ml was completed in the next 10 min and there were no further haemodynamic problems. The level of sensory block to sharp pain in our patient was at T9. The level of sympathetic block may have been 3–6 segments higher. In retrospect, the dose of bupivacaine could have been reduced, adequate preloading could have been ensured and auto transfusion could have been quickly achieved by elevating the legs. These might have avoided or terminated the laryngospasm swiftly. In conclusion, our case report demonstrates that increased vagal tone during subarachnoid block can have non-classical presentations. This is the first report of laryngospasm during subarachnoid block. The importance of fluid loading at the time of central neuraxial block needs to be emphasized. Download .zip (.0 MB) Help with zip files Download .zip (.0 MB) Help with zip files Download .zip (.0 MB) Help with zip files Download .zip (.0 MB) Help with zip files" @default.
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