Letters to Editor 5.
Suzanna AB, Liu CY, Rozaidi SW, Ooi JS. Comparison between LMA-Classic and AMBU Aura Once laryngeal mask airway in patients undergoing elective general anaesthesia with positive pressure ventilation. Med J Malaysia 2011; 66: 304-7. Access this article online Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.130126
Erdheim — Chester disease: Clinical pearls for the anesthesiologist Sir, Erdheim–Chester disease (ECD)[1] is an extremely rare non-Langerhan’s form of histiocytosis, characterized by xanthomatous tissue infiltration with foamy CD68/CD1a histiocytes. Its prompt preoperative recognition and evaluation of all the involved systems is the key to successful perioperative outcome. Approximately half of these patients have extraskeletal manifestations, including exophthalmos,[2] xanthelasma, interstitial lung disease,[3] retroperitoneal “fibrosis” with perirenal or ureteral obstruction, renal failure, diabetes insipidus, as well as central nervous system[4] and cardiovascular involvement.[5] The diagnosis of ECD can be difficult because of the rarity of the disease and the need to differentiate it from Langerhan cell histiocytosis[6] and Rosai–Dorfman disease.[7] A 66-year-old male patient presented with right ankle fracture for open reduction and internal fixation. He was a diagnosed and treated case of ECD, with severe bilateral exophthalmos (right > left). On preoperative evaluation, all routine blood investigations, including thyroid function test and coagulation profile were within normal limits. Electrocardiogram (ECG), chest X-ray, pulmonary function tests (PFT), and ultrasound abdomen were within normal limits. Whole body bone scan revealed increased radiotracer uptake in several long bones. Biopsy of the eye mass done previously showed numerous foamy histiocytes and plasma cells. Immunohistochemical stains were strongly positive for CD 68. Both eyes show axial proptosis, with bilateral multinodular mass (noncompressible, painless, nonpulsatile) in inferotemporal part of the orbit,
restricted ocular movements, bilateral cataract, and bilateral disc edema on fundus examination. In cardiac evaluation, baseline echocardiography was normal (ejection fraction 55%). Stress test (dobutamine stress echocardiography) was negative for reversible myocardial infarction. Intraoperatively, combined spinal–epidural anesthesia was administered under all asepsis. Epidural infusion was started with 0.125% bupivacaine and continued for postoperative analgesia. Special precautions were taken to protect the eyes, bony prominences, and pressure points. All vital parameters, including ECG and urine output were normal. The patient was shifted to surgical intensive care unit for observation and later shifted to ward. He was finally discharged after 2 days with advice regarding regular follow up with the orthopedic surgeon, ophthalmologist, and cardiologist. In brief, the perioperative: precautions to be taken in a patient of ECD include preoperative PFT evaluation, postoperative incentive spirometry and physiotherapy, identification of the extent of renal function derangement and choice of anesthetic agents accordingly; preparedness to perform dialysis in the perioperative period if needed, close monitoring for conduction blocks and pericardial effusion or tamponade, strict monitoring of intake–output and early identification of diabetes insipidus, gentle handling of patient; padding of pressure points and bony prominences; evaluation of the spine for any deformity, especially before attempting regional blocks, preoperative ophthalmologic assessment to document degree of vision loss and optic nerve compression; and avoidance of raised intraocular pressure and eye injuries. To conclude, the multisystem presentation of ECD can pose a challenge for the anesthesiologist, especially if not aware of its problems. Uma Hariharan, Anu Vijayant Goel1, Dhirja Sharma1 Department of Onco-Anaesthesia, Rajiv Gandhi Cancer Institute and Research Center, Rohini, 1Department of Anaesthesia, Pain and Surgi-
cal Intensive Care, Max Superspeciality Hospital, Shalimar Bagh, New Delhi, India Address for correspondence: Dr. Uma Hariharan, Department of Onco-Anaesthesia, Rajiv Gandhi Cancer Institute and Research Center, Rohini, New Delhi - 110 085, India. E-mail: [email protected]
References 1.
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Veyssier-Belot C, Cacoub P, Caparros-Lefebvre D, Wechsler J, Brun B, Remy M, et al. Erdheim-Chester disease. Clinical 297
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
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.
Suzanna AB, Liu CY, Rozaidi SW, Ooi JS. Comparison between LMA-Classic and AMBU Aura Once laryngeal mask airway in patients undergoing elective general anaesthesia with positive pressure ventilation. Med J Malaysia 2011; 66: 304-7. Access this article online Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.130126
Erdheim — Chester disease: Clinical pearls for the anesthesiologist Sir, Erdheim–Chester disease (ECD)[1] is an extremely rare non-Langerhan’s form of histiocytosis, characterized by xanthomatous tissue infiltration with foamy CD68/CD1a histiocytes. Its prompt preoperative recognition and evaluation of all the involved systems is the key to successful perioperative outcome. Approximately half of these patients have extraskeletal manifestations, including exophthalmos,[2] xanthelasma, interstitial lung disease,[3] retroperitoneal “fibrosis” with perirenal or ureteral obstruction, renal failure, diabetes insipidus, as well as central nervous system[4] and cardiovascular involvement.[5] The diagnosis of ECD can be difficult because of the rarity of the disease and the need to differentiate it from Langerhan cell histiocytosis[6] and Rosai–Dorfman disease.[7] A 66-year-old male patient presented with right ankle fracture for open reduction and internal fixation. He was a diagnosed and treated case of ECD, with severe bilateral exophthalmos (right > left). On preoperative evaluation, all routine blood investigations, including thyroid function test and coagulation profile were within normal limits. Electrocardiogram (ECG), chest X-ray, pulmonary function tests (PFT), and ultrasound abdomen were within normal limits. Whole body bone scan revealed increased radiotracer uptake in several long bones. Biopsy of the eye mass done previously showed numerous foamy histiocytes and plasma cells. Immunohistochemical stains were strongly positive for CD 68. Both eyes show axial proptosis, with bilateral multinodular mass (noncompressible, painless, nonpulsatile) in inferotemporal part of the orbit,
restricted ocular movements, bilateral cataract, and bilateral disc edema on fundus examination. In cardiac evaluation, baseline echocardiography was normal (ejection fraction 55%). Stress test (dobutamine stress echocardiography) was negative for reversible myocardial infarction. Intraoperatively, combined spinal–epidural anesthesia was administered under all asepsis. Epidural infusion was started with 0.125% bupivacaine and continued for postoperative analgesia. Special precautions were taken to protect the eyes, bony prominences, and pressure points. All vital parameters, including ECG and urine output were normal. The patient was shifted to surgical intensive care unit for observation and later shifted to ward. He was finally discharged after 2 days with advice regarding regular follow up with the orthopedic surgeon, ophthalmologist, and cardiologist. In brief, the perioperative: precautions to be taken in a patient of ECD include preoperative PFT evaluation, postoperative incentive spirometry and physiotherapy, identification of the extent of renal function derangement and choice of anesthetic agents accordingly; preparedness to perform dialysis in the perioperative period if needed, close monitoring for conduction blocks and pericardial effusion or tamponade, strict monitoring of intake–output and early identification of diabetes insipidus, gentle handling of patient; padding of pressure points and bony prominences; evaluation of the spine for any deformity, especially before attempting regional blocks, preoperative ophthalmologic assessment to document degree of vision loss and optic nerve compression; and avoidance of raised intraocular pressure and eye injuries. To conclude, the multisystem presentation of ECD can pose a challenge for the anesthesiologist, especially if not aware of its problems. Uma Hariharan, Anu Vijayant Goel1, Dhirja Sharma1 Department of Onco-Anaesthesia, Rajiv Gandhi Cancer Institute and Research Center, Rohini, 1Department of Anaesthesia, Pain and Surgi-
cal Intensive Care, Max Superspeciality Hospital, Shalimar Bagh, New Delhi, India Address for correspondence: Dr. Uma Hariharan, Department of Onco-Anaesthesia, Rajiv Gandhi Cancer Institute and Research Center, Rohini, New Delhi - 110 085, India. E-mail: [email protected]
References 1.
Journal of Anaesthesiology Clinical Pharmacology | April-June 2014 | Vol 30 | Issue 2
Veyssier-Belot C, Cacoub P, Caparros-Lefebvre D, Wechsler J, Brun B, Remy M, et al. Erdheim-Chester disease. Clinical 297
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
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.
