Letters to Editor
2.
3.
4.
5.
6. 7.
and radiologic characteristics of 59 cases. Medicine (Baltimore) 1996;75:157-69. Röpke E, Herde J, Bloching M. Erdheim-Chester disease as differential diagnosis in bilateral exophthalmos. [Article in German]. Klin Monbl Augenheilkd 2004;221:960-3. Rush WL, Andriko JA, Galateau-Salle F, Brambilla E, Brambilla C, Ziany-Bey I, et al. Pulmonary pathology of Erdheim-Chester disease. Mod Pathol 2000;13:747-54. Weidauer S, von Stuckrad-Barre S, Dettmann E, Zanella FE, Lanfermann H. Cerebral Erdheim-Chester disease: Case report and review of the literature. Neuroradiology 2003;45:241-5. Haroche J, Amoura Z, Dion E, Wechsler B, Costedoat-Chalumeau N, Cacoub P, et al. Cardiovascular involvement, an overlooked feature of Erdheim-Chester disease: Report of 6 new cases and a literature review. Medicine (Baltimore) 2004;83:371-92. Oktar N. Langerhans’ Cells may be linked to neuro-immunomodulation. J Neurol Sci 2007;24:1-4. Wright DH, Richards DB. Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): Report of a case with widespread nodal and extra nodal dissemination. Histopathology 1981;5:697-709. Access this article online Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.130127
Ascaris: An unusual cause of airway obstruction during general anesthesia with ProSeal laryngeal mask airway Sir, Airway obstruction is a potential life-threatening event that requires expeditious intervention. Identification of the cause of obstruction can be very perplexing. We describe a case of airway obstruction by a nematode in a young girl undergoing surgery under general anesthesia with ProSeal laryngeal mask airway (PLMA). A 20-year-old, 32 kg, 142 cm female was scheduled for right elbow arthroplasty. Preanesthetic assessment was normal. Preoperative heart rate (HR) was 70/minute, blood pressure (BP) 120/70 mmHg. Anesthesia was induced with fentanyl and propofol, and PLMA size 3 placement was facilitated with vecuronium and maintained with isoflurane 0.6% in oxygen (O2) and nitrous oxide (N2O). Surgery commenced after tourniquet inflation. The patient was stable with HR 298
79/minute, BP 100/50 (67) mmHg, hemoglobin oxygen saturation (SpO2) 98%, end-tidal carbon dioxide (EtCO2) 34 mmHg, and airway pressure (Paw) 13 cm H2O. One hour later, SpO2 decreased to 93%. Fraction of inspired oxygen (FiO2) was increased to 0.5, but as the SpO2 further dropped to 90%, FiO2 was maximized to 1.0. Manual bag ventilation was instituted, and PLMA position was adjusted. Bag compliance was very poor, and auscultation of the chest revealed markedly decreased air entry in the left chest. Normal EtCO2 waveform was present. SpO2 further decreased to 84% with loss of EtCO2 waveform. The PLMA was immediately removed, and manual face mask ventilation was attempted. Mask ventilation was not possible, and SpO2 was 56%. The trachea was intubated orally with a 6.5 mm cuffed tracheal tube. Bag compliance continued to be poor, Paw was 28 cm H2O, and markedly decreased air entry on left chest persisted. At this stage, HR was 98-100/minute, BP: 135-126/81-74 mmHg, SpO2: 98%-99% with FiO2 1.0 and isoflurane 0.8%-1%. Paw varied between 15 and 36 cm H2O. Twenty minutes later, frank crepitations were evident bilaterally with bloody secretions in the tracheal tube (pulmonary edema). Furosemide 15 mg and morphine 3 mg were administered intravenously (IV). HR was 83/ minute, BP: 139/79 (95) mmHg, SpO2: 98%, and Paw: 23-24 cm H2O, and multiple atrial ectopics were evident on electrocardiography (ECG). The bladder was catheterized, and the tourniquet was deflated (tourniquet time: 1 hour 53 minutes). Six minutes later, SpO2 decreased to 81% despite an FiO2 of 1.0. Isoflurane was discontinued, and furosemide 10 mg and morphine 1.5 mg were repeated. Total urine output was 300 mL over 3 hours. Cardiologist evaluation ruled out a cardiac-related cause. Positive end-expiratory pressure (PEEP) 5 cm H2O was instituted as SpO2 ranged between 85% and 94% with FiO2 1.0. The patient was transferred to the intensive care unit (ICU) on controlled ventilation, FiO2 1.0, SpO2 96%-98%, paralyzed and sedated. In the ICU, the patient was on controlled ventilation (PEEP: 5 cm H2O). Over the next six hours, saturation improved (> 95%, FiO2: 0.4) and Paw decreased (46 to 28 cm H 2O). Arterial blood gas (ABG) revealed respiratory acidosis. Chest X-ray was suggestive of left lower lung zone collapse [Figure 1]. Air entry continued to be markedly decreased on the left side on day 2. Echocardiogram was normal. On day 3, muscle paralysis was discontinued. The patient was put on synchronized intermittent mandatory ventilation (SIMV) mode (PEEP: 5 cm H2O). Fiberoptic bronchoscopic (FOB) suction was done. No other abnormality was detected. Day 4 was characterized by marked tachycardia and varying Paw. On day 5, the patient again developed pulmonary edema that
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Letters to Editor
responded to treatment. On day 6, an elongated material was spotted in the tracheal tube. An ascaris worm of length 16 cm was suctioned out [Figure 2]. Albendazole 400 mg was administered. Over the next two days, air entry became bilaterally equal. On day 10, the trachea was extubated. Patient maintained well on ventimask (FiO2: 0.4). Airway obstruction (including fatal and near-fatal cases) due to ascaris worm has been reported previously.[1-3] In the present case, we believe that the ascaris worm traveled retrograde through the esophagus into the mask of the PLMA and thence into the trachea and the left main bronchus. Review of the data on the monitor in retrospect revealed a rise in airway pressure to 43 cm H2O that went unnoticed. This probably occurred due to the presence of the worm in the trachea on its way to the left bronchus. Obstruction of the left main bronchus resulted in decreased air entry into the left chest and fall in SpO2 to 84%. Migration back into the trachea resulted in the inability to ventilate the lungs via the PLMA with loss of EtCO2 trace. This was further confirmed by the inability to manually ventilate the lungs by
face mask after removal of the PLMA and drop of SpO2 to 56%. Intubation of the trachea probably pushed the worm back into the left bronchus. Worm migration may be triggered by anesthetic agents, fever, sepsis, debilitating illness, subtherapeutic antihelminthic therapy, or by use of certain antihelminthics (pyrantel pamoate).[3] In the present case, worm migration was facilitated by lower esophageal sphincter incompetence due to anesthesia and the presence of the gastric tube. Pulmonary edema could be the result of re-expansion of the lungs following removal of the obstruction (worm migration).[4] Re-expansion pulmonary edema usually manifests following lung collapse of more than three days. However, a more acute form of reexpansion pulmonary edema, only two hours after atelectasis, during thoracic stage of esophagectomy has been reported.[5] Ravin et al.[6] reported unilateral pulmonary edema, after re-expansion of an atelectatic lung of a short duration, due to accidental placement of the tracheal tube in the right main bronchus. Alternatively, it could be because of the release of chemicals by the adult worm in the lungs that caused a reactive allergic response in the pulmonary tissue. Though rare, there should be a high index of suspicion of ascaris worm as a cause of airway obstruction especially in patients living in areas of endemic parasitic infestation. In a ventilated patient, any suspicion of a foreign body should be evaluated early by flexible fiberoptic bronchoscopy, and therapeutic rigid bronchoscopy may be necessary. Smita Prakash, Narayanan Sitalakshmi, Jasmeet Singh, Madhu Dayal, Anoop R Gogia Department of Anesthesia and Intensive Care, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India Address for correspondence: Dr. Smita Prakash, Department of Anesthesia and Intensive Care, C-17 HUDCO Place, New Delhi - 110 049, India. E-mail: [email protected]
Figure 1: Chest X-ray showing collapse of the left middle and lower lung zones
References 1.
2.
3.
4. Figure 2: Ascaris worm suctioned out of the tracheal tube
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Roy K, Kundra P, Ravishankar M. Unusual foreign body airway obstruction after laryngeal mask airway insertion. Anesth Analg 2005;101:294-5. Ramchander V, Ramcharan J, Muralidhara K. Fatal respiratory obstruction due to Ascaris lumbricoides — A case report. Ann Trop Paediatr 1991;11:293-4. Husain SJ, Zubairi AB, Sultan N, Beg MA, Mehraj V. Recurrent episodes of upper airway blockage associated with Ascaris lumbricoides causing cardiopulmonary arrest in a young patient. BMJ Case Rep 2009;2009. Khurana H, Chauhan H, Prabhakar H. Ipsilateral re-expansion pulmonary edema in a neurosurgical patient — A case report. Middle East J Anesthesiol 2008;19:1391-5. 299
Letters to Editor 5. 6.
Waller DA, Turner N. Re-expansion pulmonary oedema. Anaesthesia 1989;44:446-7. Ravin CE, Dahmash NS. Re-expansion pulmonary edema. Chest 1980;77:709-10. Access this article online
Identifying the possible cause of laryngospasm correctly is challenging.[3] General anesthesia predisposes to gastric regurgitation and aspiration. The use of a supraglottic airway device and spontaneous ventilation dose not completely secure the airway.
Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.130129
Regurgitant food particle causing intractable laryngospasm during emergence from anesthesia Sir, Laryngospasm is a common airway related complication in routine anesthetic practice. It is characterized by persistent spasmodic closure of larynx.[1] Persistent refractory complete laryngospasm during emergence after removal of an airway device is challenging to diagnose and treat.[2] A 58-yearold male weighing 62 kg with no known comorbidities was scheduled for tendon repair of index finger under general anesthesia using ProSeal laryngeal mask airway (PLMA). He was kept fasting for solids 12 h and 3 h for clear liquids. Tab. ranitidine 150 mg and tab. metoclopromide 10 mg was given night before and the day of surgery. Intravenous ramosetron 0.3 mg was given. At the end of procedure, Ryle’s tube was suctioned via drain tube and removed noting no obvious gastric contents. At this time partial laryngospasm was noted as patient breathing spontaneously till now suddenly developed noisy breathing and loss of capnography trace. In view of PLMA being a predisposing factor for undesired airway stimulation under lighter plane of anesthesia, it was quickly removed. Patient continued to be assisted with 100% oxygen and gentle CPAP of 20 cm H2O. Within 60 s chest was seen expanding again coinciding well with reservoir bag movement and return of capnography trace. However, partial laryngospasm returned with a noisy breathing and progressed to complete laryngospasm. Upper airway obstruction was ruled out as a lubricated nasopharyngeal airway was gently inserted and showed only minimal secretions on suctioning. Once the patient became more awake, he had a sudden bout of vigorous cough and patient coughed out unidentifiable material into the face mask 300
which immediately relieved the spasm. Closer examination revealed it was an unsuspecting food particle (intact skin of a red chilly) which he probably regurgitated and was causing recurrent laryngospasm.
The technique of draining the stomach via a Ryle’s tube in a PLMA may not clear larger food particles from the stomach. Also a PLMA is associated with variable amount of gastric insufflation.[4] In our case regurgitation may have occurred at the end of procedure, in a lighter plane of anesthesia. Presence of a nasogastric tube in situ itself may act as a stimulant for regurgitation since lower esophageal sphincter remains patent. Laryngospasm was refractory to treatment. Only on return of cough reflex was the patient able to expel the food material which is the likely culprit of recurrent laryngospasm. The likelihood of regurgitation is high even in an adequately fasting patient. Laryngospasm may often be an early feature of pulmonary aspiration. A history of gastroesophageal reflux may indicate more chances of developing laryngospasm under general anesthesia. Thus, in presence of recurrent intractable laryngospasm; the possibility of regurgitant food particles persistently irritating the larynx should be thought of early. Mouveen Sharma, Tim Thomas Joseph, Souvik Chaudhuri, Amrut K Rao Department of Anesthesiology, Kasturba Medical College, Manipal University, Manipal, Karnataka, India Address for correspondence: Dr. Tim Thomas Joseph, Department of Anaesthesiology, Kasturba Medical College, Manipal - 576 104, Karnataka, India. E-mail: [email protected]
References 1.
2.
3.
Salem MR, Ramez M, Crystal GJ, Nimmagadda U. Understanding the mechanics of laryngospasm is crucial for proper treatment. Anesthesiology 2012;117:441-2. Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: Laryngospasm. Qual Saf Health Care 2005;14:e3. Baduni N, Sanwal MK, Jain A, Kachru N. Recurrent episodes of intractable laryngospasm followed by laryngeal and pulmonary oedema during dissociative anaesthesiawith intravenous ketamine. Indian J Anaesth 2010;54:364-5.
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Copyright of Journal of Anaesthesiology Clinical Pharmacology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
2.
3.
4.
5.
6. 7.
and radiologic characteristics of 59 cases. Medicine (Baltimore) 1996;75:157-69. Röpke E, Herde J, Bloching M. Erdheim-Chester disease as differential diagnosis in bilateral exophthalmos. [Article in German]. Klin Monbl Augenheilkd 2004;221:960-3. Rush WL, Andriko JA, Galateau-Salle F, Brambilla E, Brambilla C, Ziany-Bey I, et al. Pulmonary pathology of Erdheim-Chester disease. Mod Pathol 2000;13:747-54. Weidauer S, von Stuckrad-Barre S, Dettmann E, Zanella FE, Lanfermann H. Cerebral Erdheim-Chester disease: Case report and review of the literature. Neuroradiology 2003;45:241-5. Haroche J, Amoura Z, Dion E, Wechsler B, Costedoat-Chalumeau N, Cacoub P, et al. Cardiovascular involvement, an overlooked feature of Erdheim-Chester disease: Report of 6 new cases and a literature review. Medicine (Baltimore) 2004;83:371-92. Oktar N. Langerhans’ Cells may be linked to neuro-immunomodulation. J Neurol Sci 2007;24:1-4. Wright DH, Richards DB. Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): Report of a case with widespread nodal and extra nodal dissemination. Histopathology 1981;5:697-709. Access this article online Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.130127
Ascaris: An unusual cause of airway obstruction during general anesthesia with ProSeal laryngeal mask airway Sir, Airway obstruction is a potential life-threatening event that requires expeditious intervention. Identification of the cause of obstruction can be very perplexing. We describe a case of airway obstruction by a nematode in a young girl undergoing surgery under general anesthesia with ProSeal laryngeal mask airway (PLMA). A 20-year-old, 32 kg, 142 cm female was scheduled for right elbow arthroplasty. Preanesthetic assessment was normal. Preoperative heart rate (HR) was 70/minute, blood pressure (BP) 120/70 mmHg. Anesthesia was induced with fentanyl and propofol, and PLMA size 3 placement was facilitated with vecuronium and maintained with isoflurane 0.6% in oxygen (O2) and nitrous oxide (N2O). Surgery commenced after tourniquet inflation. The patient was stable with HR 298
79/minute, BP 100/50 (67) mmHg, hemoglobin oxygen saturation (SpO2) 98%, end-tidal carbon dioxide (EtCO2) 34 mmHg, and airway pressure (Paw) 13 cm H2O. One hour later, SpO2 decreased to 93%. Fraction of inspired oxygen (FiO2) was increased to 0.5, but as the SpO2 further dropped to 90%, FiO2 was maximized to 1.0. Manual bag ventilation was instituted, and PLMA position was adjusted. Bag compliance was very poor, and auscultation of the chest revealed markedly decreased air entry in the left chest. Normal EtCO2 waveform was present. SpO2 further decreased to 84% with loss of EtCO2 waveform. The PLMA was immediately removed, and manual face mask ventilation was attempted. Mask ventilation was not possible, and SpO2 was 56%. The trachea was intubated orally with a 6.5 mm cuffed tracheal tube. Bag compliance continued to be poor, Paw was 28 cm H2O, and markedly decreased air entry on left chest persisted. At this stage, HR was 98-100/minute, BP: 135-126/81-74 mmHg, SpO2: 98%-99% with FiO2 1.0 and isoflurane 0.8%-1%. Paw varied between 15 and 36 cm H2O. Twenty minutes later, frank crepitations were evident bilaterally with bloody secretions in the tracheal tube (pulmonary edema). Furosemide 15 mg and morphine 3 mg were administered intravenously (IV). HR was 83/ minute, BP: 139/79 (95) mmHg, SpO2: 98%, and Paw: 23-24 cm H2O, and multiple atrial ectopics were evident on electrocardiography (ECG). The bladder was catheterized, and the tourniquet was deflated (tourniquet time: 1 hour 53 minutes). Six minutes later, SpO2 decreased to 81% despite an FiO2 of 1.0. Isoflurane was discontinued, and furosemide 10 mg and morphine 1.5 mg were repeated. Total urine output was 300 mL over 3 hours. Cardiologist evaluation ruled out a cardiac-related cause. Positive end-expiratory pressure (PEEP) 5 cm H2O was instituted as SpO2 ranged between 85% and 94% with FiO2 1.0. The patient was transferred to the intensive care unit (ICU) on controlled ventilation, FiO2 1.0, SpO2 96%-98%, paralyzed and sedated. In the ICU, the patient was on controlled ventilation (PEEP: 5 cm H2O). Over the next six hours, saturation improved (> 95%, FiO2: 0.4) and Paw decreased (46 to 28 cm H 2O). Arterial blood gas (ABG) revealed respiratory acidosis. Chest X-ray was suggestive of left lower lung zone collapse [Figure 1]. Air entry continued to be markedly decreased on the left side on day 2. Echocardiogram was normal. On day 3, muscle paralysis was discontinued. The patient was put on synchronized intermittent mandatory ventilation (SIMV) mode (PEEP: 5 cm H2O). Fiberoptic bronchoscopic (FOB) suction was done. No other abnormality was detected. Day 4 was characterized by marked tachycardia and varying Paw. On day 5, the patient again developed pulmonary edema that
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Letters to Editor
responded to treatment. On day 6, an elongated material was spotted in the tracheal tube. An ascaris worm of length 16 cm was suctioned out [Figure 2]. Albendazole 400 mg was administered. Over the next two days, air entry became bilaterally equal. On day 10, the trachea was extubated. Patient maintained well on ventimask (FiO2: 0.4). Airway obstruction (including fatal and near-fatal cases) due to ascaris worm has been reported previously.[1-3] In the present case, we believe that the ascaris worm traveled retrograde through the esophagus into the mask of the PLMA and thence into the trachea and the left main bronchus. Review of the data on the monitor in retrospect revealed a rise in airway pressure to 43 cm H2O that went unnoticed. This probably occurred due to the presence of the worm in the trachea on its way to the left bronchus. Obstruction of the left main bronchus resulted in decreased air entry into the left chest and fall in SpO2 to 84%. Migration back into the trachea resulted in the inability to ventilate the lungs via the PLMA with loss of EtCO2 trace. This was further confirmed by the inability to manually ventilate the lungs by
face mask after removal of the PLMA and drop of SpO2 to 56%. Intubation of the trachea probably pushed the worm back into the left bronchus. Worm migration may be triggered by anesthetic agents, fever, sepsis, debilitating illness, subtherapeutic antihelminthic therapy, or by use of certain antihelminthics (pyrantel pamoate).[3] In the present case, worm migration was facilitated by lower esophageal sphincter incompetence due to anesthesia and the presence of the gastric tube. Pulmonary edema could be the result of re-expansion of the lungs following removal of the obstruction (worm migration).[4] Re-expansion pulmonary edema usually manifests following lung collapse of more than three days. However, a more acute form of reexpansion pulmonary edema, only two hours after atelectasis, during thoracic stage of esophagectomy has been reported.[5] Ravin et al.[6] reported unilateral pulmonary edema, after re-expansion of an atelectatic lung of a short duration, due to accidental placement of the tracheal tube in the right main bronchus. Alternatively, it could be because of the release of chemicals by the adult worm in the lungs that caused a reactive allergic response in the pulmonary tissue. Though rare, there should be a high index of suspicion of ascaris worm as a cause of airway obstruction especially in patients living in areas of endemic parasitic infestation. In a ventilated patient, any suspicion of a foreign body should be evaluated early by flexible fiberoptic bronchoscopy, and therapeutic rigid bronchoscopy may be necessary. Smita Prakash, Narayanan Sitalakshmi, Jasmeet Singh, Madhu Dayal, Anoop R Gogia Department of Anesthesia and Intensive Care, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India Address for correspondence: Dr. Smita Prakash, Department of Anesthesia and Intensive Care, C-17 HUDCO Place, New Delhi - 110 049, India. E-mail: [email protected]
Figure 1: Chest X-ray showing collapse of the left middle and lower lung zones
References 1.
2.
3.
4. Figure 2: Ascaris worm suctioned out of the tracheal tube
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Roy K, Kundra P, Ravishankar M. Unusual foreign body airway obstruction after laryngeal mask airway insertion. Anesth Analg 2005;101:294-5. Ramchander V, Ramcharan J, Muralidhara K. Fatal respiratory obstruction due to Ascaris lumbricoides — A case report. Ann Trop Paediatr 1991;11:293-4. Husain SJ, Zubairi AB, Sultan N, Beg MA, Mehraj V. Recurrent episodes of upper airway blockage associated with Ascaris lumbricoides causing cardiopulmonary arrest in a young patient. BMJ Case Rep 2009;2009. Khurana H, Chauhan H, Prabhakar H. Ipsilateral re-expansion pulmonary edema in a neurosurgical patient — A case report. Middle East J Anesthesiol 2008;19:1391-5. 299
Letters to Editor 5. 6.
Waller DA, Turner N. Re-expansion pulmonary oedema. Anaesthesia 1989;44:446-7. Ravin CE, Dahmash NS. Re-expansion pulmonary edema. Chest 1980;77:709-10. Access this article online
Identifying the possible cause of laryngospasm correctly is challenging.[3] General anesthesia predisposes to gastric regurgitation and aspiration. The use of a supraglottic airway device and spontaneous ventilation dose not completely secure the airway.
Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.130129
Regurgitant food particle causing intractable laryngospasm during emergence from anesthesia Sir, Laryngospasm is a common airway related complication in routine anesthetic practice. It is characterized by persistent spasmodic closure of larynx.[1] Persistent refractory complete laryngospasm during emergence after removal of an airway device is challenging to diagnose and treat.[2] A 58-yearold male weighing 62 kg with no known comorbidities was scheduled for tendon repair of index finger under general anesthesia using ProSeal laryngeal mask airway (PLMA). He was kept fasting for solids 12 h and 3 h for clear liquids. Tab. ranitidine 150 mg and tab. metoclopromide 10 mg was given night before and the day of surgery. Intravenous ramosetron 0.3 mg was given. At the end of procedure, Ryle’s tube was suctioned via drain tube and removed noting no obvious gastric contents. At this time partial laryngospasm was noted as patient breathing spontaneously till now suddenly developed noisy breathing and loss of capnography trace. In view of PLMA being a predisposing factor for undesired airway stimulation under lighter plane of anesthesia, it was quickly removed. Patient continued to be assisted with 100% oxygen and gentle CPAP of 20 cm H2O. Within 60 s chest was seen expanding again coinciding well with reservoir bag movement and return of capnography trace. However, partial laryngospasm returned with a noisy breathing and progressed to complete laryngospasm. Upper airway obstruction was ruled out as a lubricated nasopharyngeal airway was gently inserted and showed only minimal secretions on suctioning. Once the patient became more awake, he had a sudden bout of vigorous cough and patient coughed out unidentifiable material into the face mask 300
which immediately relieved the spasm. Closer examination revealed it was an unsuspecting food particle (intact skin of a red chilly) which he probably regurgitated and was causing recurrent laryngospasm.
The technique of draining the stomach via a Ryle’s tube in a PLMA may not clear larger food particles from the stomach. Also a PLMA is associated with variable amount of gastric insufflation.[4] In our case regurgitation may have occurred at the end of procedure, in a lighter plane of anesthesia. Presence of a nasogastric tube in situ itself may act as a stimulant for regurgitation since lower esophageal sphincter remains patent. Laryngospasm was refractory to treatment. Only on return of cough reflex was the patient able to expel the food material which is the likely culprit of recurrent laryngospasm. The likelihood of regurgitation is high even in an adequately fasting patient. Laryngospasm may often be an early feature of pulmonary aspiration. A history of gastroesophageal reflux may indicate more chances of developing laryngospasm under general anesthesia. Thus, in presence of recurrent intractable laryngospasm; the possibility of regurgitant food particles persistently irritating the larynx should be thought of early. Mouveen Sharma, Tim Thomas Joseph, Souvik Chaudhuri, Amrut K Rao Department of Anesthesiology, Kasturba Medical College, Manipal University, Manipal, Karnataka, India Address for correspondence: Dr. Tim Thomas Joseph, Department of Anaesthesiology, Kasturba Medical College, Manipal - 576 104, Karnataka, India. E-mail: [email protected]
References 1.
2.
3.
Salem MR, Ramez M, Crystal GJ, Nimmagadda U. Understanding the mechanics of laryngospasm is crucial for proper treatment. Anesthesiology 2012;117:441-2. Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: Laryngospasm. Qual Saf Health Care 2005;14:e3. Baduni N, Sanwal MK, Jain A, Kachru N. Recurrent episodes of intractable laryngospasm followed by laryngeal and pulmonary oedema during dissociative anaesthesiawith intravenous ketamine. Indian J Anaesth 2010;54:364-5.
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Copyright of Journal of Anaesthesiology Clinical Pharmacology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
