Letters to Editor
and pain on the visual analog scale (VAS) varied between 30 and 70/100. Physical examination revealed extensive HS over the burnt area. The sensations over the affected area were normal without any static mechanical allodynia (allodynia to touch and pressure). The scar was too extensive to consider any local therapy (e.g., steroid infiltration within the scar). The cosmetic deformity was not an issue for the patient so a decision to start systemic therapy with tablet pregabalin and amitriptyline was made. Pregabalin was advised 75 mg in the night for 3 days and then twice a day thereafter. Amitriptyline was advised in the dose of 10 mg in the night for 1 week followed by 25 mg thereafter. Patient was kept on a fortnightly follow-up. Patient showed a significant improvement in symptoms within 5 days with progressive improvement in symptoms as the treatment proceeded. At 3 months since the start of treatment patient has shown progressive improvement and is now pursuing his occupation and has started socializing with friends. His sleep has normalized and he is much less irritable. While on medicines the DN4 score was 0/10 and VAS was 10/100. Neuropathic pain has always been a difficult to treat in comparison with the nociceptive pain. Diabetic neuropathy and neuropathic pain associated with it has been the basis of treatment of the neuropathic pain in other disorders. We propose that systemic medical therapy using standard anti-neuropathic medications may be effective in treating pain in HS. Pregabalin by binding to the α2δ subunit of the voltage-dependent calcium channel in the central nervous system decreases the release of neurotransmitters including glutamate, noradrenaline, substance P and calcitonin generelated peptide.[3] Amitriptyline inhibit sodium channels and L-type calcium channels, inhibits serotonin-norepinephrine reuptake by blocking the serotonin transporter and the norepinephrine transporter leading to elevation of the synaptic concentrations of these neurotransmitters, thus an enhancement of neurotransmission in the descending pain modulating pathway.[4] Although pharmacotherapy is essential for management of HS pain, the role of psychotherapy in the form of a variety of cognitive-behavioral therapies including distraction, imagery, biofeedback or hypnotic analgesia provided by trained staff cannot be underemphasized. 112
Anuj Jain, Anil Agarwal, Chetna Shamshery Department of Anesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India Address for correspondence: Dr. Anuj Jain, Department of Anesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India. E-mail: [email protected]
References 1.
2.
3.
4.
Isoardo G, Stella M, Cocito D, Risso D, Migliaretti G, Cauda F, et al. Neuropathic pain in post-burn hypertrophic scars: A psychophysical and neurophysiological study. Muscle Nerve 2012;45:883-90. Kawecki M, Bernad-Wiśniewska T, Sakiel S, Nowak M, Andriessen A. Laser in the treatment of hypertrophic burn scars. Int Wound J 2008;5:87-9. Micheva KD, Taylor CP, Smith SJ. Pregabalin reduces the release of synaptic vesicles from cultured hippocampal neurons. Mol Pharmacol 2006;70:467-76. Gillman PK. Tricyclic antidepressant pharmacology and therapeutic drug interactions updated. Br J Pharmacol 2007;151:737-48. Access this article online Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.125721
Transient compressive lumbar radiculopathy following post-epidural blood patch Sir, Post-dural-puncture-headache is a common complication seen after an intentional or an accidental breach of the dura mater at the spinal level. Epidural blood patch (EBP) is a commonly utilized interventional modality for treating difficultto-intractable headache after a dural puncture. However, in comparison with the reports about the success rates of EBP, the complications and concerns related to EBP as an intervention itself have been rarely reported.[1] We hereby present a case wherein, our patient was re-admitted to the emergency room due to radicular pains after a successful EBP. A 20-year-old female patient presented to the emergency room with the chief complaint of intermittent and shooting low back pain, radiating bilaterally to buttocks and knees. Four days prior, she had undergone a continuous labor epidural
Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1
Letters to Editor
placement, complicated by post-dural-puncture-headache that was most likely secondary to unrecognized dural puncture during epidural placement. Subsequently, she had received an EBP with 20 mL autologous blood. She had not reported pain or neurological symptoms during EBP placement. Her back pain had started 48 h after EBP placement. Emergent magnetic resonance imaging (MRI) of the lumbosacral spine revealed small amounts of clear fluid with hemorrhagic components in posterior lumbar epidural space, associated with thecal sac compression [Figure 1]. Neurosurgery team recommended conservative management. Patient was discharged home with analgesics and advised regular follow-up. Back pain following neuraxial procedures (including EBP) is secondary to procedural technique, irritant medications as well as due to compression secondary to fluid collection.[2,3] In patients with non-resolving or worsening back pain or neurological symptoms, lumbosacral MRI may be essential to rule out significant post-EBP complications such as intrathecal hematoma,[4] cauda equina syndrome,[4] spinal subdural hematoma[3] and epidural abscess.[2,4] In contrast to our patient’s presentation, these catastrophic complications usually have rapidly-progressive course with worsening sensorimotor deficits and bladder-bowel dysfunction unless an early diagnosis with MRI and timely neurosurgical intervention ensue.[2] In our patient, fluid with blood components was confined to posterior epidural space without any apparent subdural or intrathecal extensions of injected blood ruling out the above mentioned catastrophic complications of EBP. In addition based on her symptoms, non-infectious (inflammatory) arachnoiditis was considered as differential diagnosis, but the definitive radiological signs for arachnoiditis[5] (loculated subarachnoid space, clumped nerve roots with “empty-sac” sign) were not present. Hence, we concluded that our patient developed compressive lumbar radiculopathy secondary to standard volume (20 mL) EBP
unlike as reported with large volume (40 mL) EBP by Desai et al.[3] Although Beards et al. had demonstrated that only small clots were visible 18 h following EBP injection,[6] our patient demonstrated blood (injected component) with cerebrospinal fluid (leakage component) within the epidural space, even 48 h following EBP. However, it cannot be ruled out that the fluid component visible on MRI was secondary to the onset of clot organization with liquefaction in the epidural space because EBP induces accelerated coagulation mechanisms in the region of cerebrospinal fluid leak.[6] In summary, although immediate but transient radicular symptoms during EBP placement have been used as cut-off for injected blood volume’s therapeutic adequacy and safety, [7,8] persistent radicular symptoms in postEBP patients act as warning signals for compressive lumbar radiculopathy that requires active interventions including analgesics and steroidal medications[3] as well as neurosurgical consultation. Deepak Gupta, Hassan Amhaz, Ashish Mazumdar, Vitaly Soskin Department of Anesthesiology, Wayne State University/Detroit Medical Center, Detroit, MI, USA Address for correspondence: Dr. Vitaly Soskin, Department of Anesthesiology, Wayne State University, School of Medicine, Box No. 162, 3990 John R, Detroit, MI 48201, USA. E-mail: [email protected]
References 1. 2.
3.
4.
5.
Figure 1: T2-weighted magnetic resonance imaging: Axial image (image on the left side) at second lumbar vertebral body (L2) and sagittal image (image on the right side) of the lumbosacral spine demonstrating diffuse, but mild thecal compression secondary to the collection in the posterior epidural space; limits of this epidural space collection (inhomogeneous foci representing blood-mixed cerebrospinal fluid) is marked by (←) in axial image for its side-to-side extent and by (←) in sagittal image for its posterior extent. Incidental finding of transitional fifth lumbar vertebra marked as L5
6.
7.
Weakland HJ. The epidural blood patch — Current practices and concerns. CRNA 1994;5:156-63. Nysora.com [homepage on the Interne]. Epidural blockade [about 1 screen]. New York: The New York School of Regional Anesthesia (NYSORA, Inc.); 1996, 2012. Available from: http://www.nysora. com/regional_anesthesia/neuraxial_techniques/3026-epiduralblockade.html. [Updated on 2009 Jan 3; Cited on 2013 Jun 10]. Desai MJ, Dave AP, Martin MB. Delayed radicular pain following two large volume epidural blood patches for post-lumbar puncture headache: A case report. Pain Physician 2010;13:257-62. Kalina P, Craigo P, Weingarten T. Intrathecal injection of epidural blood patch: A case report and review of the literature. Emerg Radiol 2004;11:56-9. Holz A, Levy LM, Coombs BD, DeLaPaz RL, Krasny RM, Smirniotopoulos JG. Arachnoiditis imaging [about 1 screen]. Emedicine.Medscape. com [homepage on the Internet]. New York: WebMD LLC; 1994-2013. Available from: http://emedicine.medscape.com/article/336605overview#a21. [Updated on 2011 May 25; Cited on 2013 Jun 10]. Beards SC, Jackson A, Griffiths AG, Horsman EL. Magnetic resonance imaging of extradural blood patches: Appearances from 30 min to 18 h. Br J Anaesth 1993;71:182-8. Szeinfeld M, Ihmeidan IH, Moser MM, Machado R, Klose KJ, Serafini AN. Epidural blood patch: Evaluation of the volume and spread of blood injected into the epidural space. Anesthesiology 1986;64:820-2.
Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1
113
Letters to Editor 8.
Mehta B, Tarshis J. Repeated large-volume epidural blood patches for the treatment of spontaneous intracranial hypotension. Can J Anaesth 2009;56:609-13.
References 1. 2.
Access this article online Quick Response Code:
Website: www.joacp.org
3.
DOI: 10.4103/0970-9185.125723
Beyaz SG. Persistent hiccup after lumbar epidural steroid injection. J Anaesthesiol Clin Pharmacol 2012;28:418-9. Beyaz SG, Tüfek A, Tokgöz O, Karaman H. A case of pneumothorax after phrenic nerve block with guidance of a nerve stimulator. Korean J Pain 2011;24:105-7. Slipman CW, Shin CH, Patel RK, Braverman DL, Lenrow DA, Ellen MI, et al. Persistent hiccup associated with thoracic epidural injection. Am J Phys Med Rehabil 2001;80:618-21. Access this article online Quick Response Code:
Reply to: Management of intraoperative hiccups with intravenous promethazine Sir, I read with pleasure the letters to the editor regarding my paper entitled “Persistent hiccups after lumbar epidural steroid injection,” which was published in your journal. The treatment of hiccups must be based on the etiology of the underlying disease. Treatment modalities may be classified as non-pharmacological, pharmacological and invasive methods. Non-pharmacological methods include holding one’s breath, drinking cold water, compression of the eyeball, carbon dioxide inhalation, nasogastric tube placement and gastric lavage.[1] The authors reported that they used some of these non-pharmacological methods in the intraoperative period; however, no benefit could be obtained. Pharmacological methods include metoclopramide, chlorpromazine, amitriptyline, phenytoin, valproic acid, baclofen and gabapentin, which are used as a monotherapy or combination therapy.[2] The authors reported that they treated hiccups that develop in the intraoperative period with a single dose of 12.5 mg promethazine. Although they reported that there was only one case report about promethazine use for the treatment of hiccups, they did not indicate any references.[3] It may be valuable for the treatment of hiccups, which develop in regional anesthesia and for a limited time during operations and which impair surgical comfort. We thank the author for their contribution. Serbülent Gökhan Beyaz Department of Anesthesiology and Reanimation, Sakarya University Medical School, Sakarya, Turkey Address for correspondence: Dr. Serbülent Gökhan Beyaz, Sakarya University Medical School, Department of Anesthesiology and Reanimation, Merkez Campus, Adnan Menderes Street, Adapazarı, Sakarya, Turkey. E-mail: [email protected] 114
Website: www.joacp.org
DOI: 10.4103/0970-9185.125724
Providing anesthesia in a remote location for radiation oncology in an adult Problems and solutions Sir, With the increasing role for anesthesiologists outside operating room locations, we are asked to provide services in unknown areas with limited resources. There is a significant mortality and morbidity associated with providing anesthesia in these locations.[1] We describe a patient successfully anesthetized in such a location (radiotherapy suite) on a daily basis for around 6 weeks. A 30-year-male (ASA III, weighing 90 kg) presented for radiation (photon beam) therapy, to treat invasive squamous cell carcinoma of the mastoid. Mild mental retardation due to cerebral palsy necessitated anesthesia to maintain immobility throughout the procedure. Although, the patient was able to understand verbal commands, he was unable to stay still for the duration of the procedure. His speech and language skills were fairly developed and communication skills were acceptable. Airway examination showed a Malampatti class 3 with adequate mouth opening and neck extension. The aims of anesthesia were to maintain spontaneous ventilation and immobility [Figure 1] without requiring significant airway intervention for the duration of the procedure. It was also important to ensure quick recovery facilitating early discharge as the procedure was planned only on an out-patient basis. After connecting to routine monitors and obtaining baseline
Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1
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.
and pain on the visual analog scale (VAS) varied between 30 and 70/100. Physical examination revealed extensive HS over the burnt area. The sensations over the affected area were normal without any static mechanical allodynia (allodynia to touch and pressure). The scar was too extensive to consider any local therapy (e.g., steroid infiltration within the scar). The cosmetic deformity was not an issue for the patient so a decision to start systemic therapy with tablet pregabalin and amitriptyline was made. Pregabalin was advised 75 mg in the night for 3 days and then twice a day thereafter. Amitriptyline was advised in the dose of 10 mg in the night for 1 week followed by 25 mg thereafter. Patient was kept on a fortnightly follow-up. Patient showed a significant improvement in symptoms within 5 days with progressive improvement in symptoms as the treatment proceeded. At 3 months since the start of treatment patient has shown progressive improvement and is now pursuing his occupation and has started socializing with friends. His sleep has normalized and he is much less irritable. While on medicines the DN4 score was 0/10 and VAS was 10/100. Neuropathic pain has always been a difficult to treat in comparison with the nociceptive pain. Diabetic neuropathy and neuropathic pain associated with it has been the basis of treatment of the neuropathic pain in other disorders. We propose that systemic medical therapy using standard anti-neuropathic medications may be effective in treating pain in HS. Pregabalin by binding to the α2δ subunit of the voltage-dependent calcium channel in the central nervous system decreases the release of neurotransmitters including glutamate, noradrenaline, substance P and calcitonin generelated peptide.[3] Amitriptyline inhibit sodium channels and L-type calcium channels, inhibits serotonin-norepinephrine reuptake by blocking the serotonin transporter and the norepinephrine transporter leading to elevation of the synaptic concentrations of these neurotransmitters, thus an enhancement of neurotransmission in the descending pain modulating pathway.[4] Although pharmacotherapy is essential for management of HS pain, the role of psychotherapy in the form of a variety of cognitive-behavioral therapies including distraction, imagery, biofeedback or hypnotic analgesia provided by trained staff cannot be underemphasized. 112
Anuj Jain, Anil Agarwal, Chetna Shamshery Department of Anesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India Address for correspondence: Dr. Anuj Jain, Department of Anesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India. E-mail: [email protected]
References 1.
2.
3.
4.
Isoardo G, Stella M, Cocito D, Risso D, Migliaretti G, Cauda F, et al. Neuropathic pain in post-burn hypertrophic scars: A psychophysical and neurophysiological study. Muscle Nerve 2012;45:883-90. Kawecki M, Bernad-Wiśniewska T, Sakiel S, Nowak M, Andriessen A. Laser in the treatment of hypertrophic burn scars. Int Wound J 2008;5:87-9. Micheva KD, Taylor CP, Smith SJ. Pregabalin reduces the release of synaptic vesicles from cultured hippocampal neurons. Mol Pharmacol 2006;70:467-76. Gillman PK. Tricyclic antidepressant pharmacology and therapeutic drug interactions updated. Br J Pharmacol 2007;151:737-48. Access this article online Quick Response Code:
Website: www.joacp.org
DOI: 10.4103/0970-9185.125721
Transient compressive lumbar radiculopathy following post-epidural blood patch Sir, Post-dural-puncture-headache is a common complication seen after an intentional or an accidental breach of the dura mater at the spinal level. Epidural blood patch (EBP) is a commonly utilized interventional modality for treating difficultto-intractable headache after a dural puncture. However, in comparison with the reports about the success rates of EBP, the complications and concerns related to EBP as an intervention itself have been rarely reported.[1] We hereby present a case wherein, our patient was re-admitted to the emergency room due to radicular pains after a successful EBP. A 20-year-old female patient presented to the emergency room with the chief complaint of intermittent and shooting low back pain, radiating bilaterally to buttocks and knees. Four days prior, she had undergone a continuous labor epidural
Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1
Letters to Editor
placement, complicated by post-dural-puncture-headache that was most likely secondary to unrecognized dural puncture during epidural placement. Subsequently, she had received an EBP with 20 mL autologous blood. She had not reported pain or neurological symptoms during EBP placement. Her back pain had started 48 h after EBP placement. Emergent magnetic resonance imaging (MRI) of the lumbosacral spine revealed small amounts of clear fluid with hemorrhagic components in posterior lumbar epidural space, associated with thecal sac compression [Figure 1]. Neurosurgery team recommended conservative management. Patient was discharged home with analgesics and advised regular follow-up. Back pain following neuraxial procedures (including EBP) is secondary to procedural technique, irritant medications as well as due to compression secondary to fluid collection.[2,3] In patients with non-resolving or worsening back pain or neurological symptoms, lumbosacral MRI may be essential to rule out significant post-EBP complications such as intrathecal hematoma,[4] cauda equina syndrome,[4] spinal subdural hematoma[3] and epidural abscess.[2,4] In contrast to our patient’s presentation, these catastrophic complications usually have rapidly-progressive course with worsening sensorimotor deficits and bladder-bowel dysfunction unless an early diagnosis with MRI and timely neurosurgical intervention ensue.[2] In our patient, fluid with blood components was confined to posterior epidural space without any apparent subdural or intrathecal extensions of injected blood ruling out the above mentioned catastrophic complications of EBP. In addition based on her symptoms, non-infectious (inflammatory) arachnoiditis was considered as differential diagnosis, but the definitive radiological signs for arachnoiditis[5] (loculated subarachnoid space, clumped nerve roots with “empty-sac” sign) were not present. Hence, we concluded that our patient developed compressive lumbar radiculopathy secondary to standard volume (20 mL) EBP
unlike as reported with large volume (40 mL) EBP by Desai et al.[3] Although Beards et al. had demonstrated that only small clots were visible 18 h following EBP injection,[6] our patient demonstrated blood (injected component) with cerebrospinal fluid (leakage component) within the epidural space, even 48 h following EBP. However, it cannot be ruled out that the fluid component visible on MRI was secondary to the onset of clot organization with liquefaction in the epidural space because EBP induces accelerated coagulation mechanisms in the region of cerebrospinal fluid leak.[6] In summary, although immediate but transient radicular symptoms during EBP placement have been used as cut-off for injected blood volume’s therapeutic adequacy and safety, [7,8] persistent radicular symptoms in postEBP patients act as warning signals for compressive lumbar radiculopathy that requires active interventions including analgesics and steroidal medications[3] as well as neurosurgical consultation. Deepak Gupta, Hassan Amhaz, Ashish Mazumdar, Vitaly Soskin Department of Anesthesiology, Wayne State University/Detroit Medical Center, Detroit, MI, USA Address for correspondence: Dr. Vitaly Soskin, Department of Anesthesiology, Wayne State University, School of Medicine, Box No. 162, 3990 John R, Detroit, MI 48201, USA. E-mail: [email protected]
References 1. 2.
3.
4.
5.
Figure 1: T2-weighted magnetic resonance imaging: Axial image (image on the left side) at second lumbar vertebral body (L2) and sagittal image (image on the right side) of the lumbosacral spine demonstrating diffuse, but mild thecal compression secondary to the collection in the posterior epidural space; limits of this epidural space collection (inhomogeneous foci representing blood-mixed cerebrospinal fluid) is marked by (←) in axial image for its side-to-side extent and by (←) in sagittal image for its posterior extent. Incidental finding of transitional fifth lumbar vertebra marked as L5
6.
7.
Weakland HJ. The epidural blood patch — Current practices and concerns. CRNA 1994;5:156-63. Nysora.com [homepage on the Interne]. Epidural blockade [about 1 screen]. New York: The New York School of Regional Anesthesia (NYSORA, Inc.); 1996, 2012. Available from: http://www.nysora. com/regional_anesthesia/neuraxial_techniques/3026-epiduralblockade.html. [Updated on 2009 Jan 3; Cited on 2013 Jun 10]. Desai MJ, Dave AP, Martin MB. Delayed radicular pain following two large volume epidural blood patches for post-lumbar puncture headache: A case report. Pain Physician 2010;13:257-62. Kalina P, Craigo P, Weingarten T. Intrathecal injection of epidural blood patch: A case report and review of the literature. Emerg Radiol 2004;11:56-9. Holz A, Levy LM, Coombs BD, DeLaPaz RL, Krasny RM, Smirniotopoulos JG. Arachnoiditis imaging [about 1 screen]. Emedicine.Medscape. com [homepage on the Internet]. New York: WebMD LLC; 1994-2013. Available from: http://emedicine.medscape.com/article/336605overview#a21. [Updated on 2011 May 25; Cited on 2013 Jun 10]. Beards SC, Jackson A, Griffiths AG, Horsman EL. Magnetic resonance imaging of extradural blood patches: Appearances from 30 min to 18 h. Br J Anaesth 1993;71:182-8. Szeinfeld M, Ihmeidan IH, Moser MM, Machado R, Klose KJ, Serafini AN. Epidural blood patch: Evaluation of the volume and spread of blood injected into the epidural space. Anesthesiology 1986;64:820-2.
Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1
113
Letters to Editor 8.
Mehta B, Tarshis J. Repeated large-volume epidural blood patches for the treatment of spontaneous intracranial hypotension. Can J Anaesth 2009;56:609-13.
References 1. 2.
Access this article online Quick Response Code:
Website: www.joacp.org
3.
DOI: 10.4103/0970-9185.125723
Beyaz SG. Persistent hiccup after lumbar epidural steroid injection. J Anaesthesiol Clin Pharmacol 2012;28:418-9. Beyaz SG, Tüfek A, Tokgöz O, Karaman H. A case of pneumothorax after phrenic nerve block with guidance of a nerve stimulator. Korean J Pain 2011;24:105-7. Slipman CW, Shin CH, Patel RK, Braverman DL, Lenrow DA, Ellen MI, et al. Persistent hiccup associated with thoracic epidural injection. Am J Phys Med Rehabil 2001;80:618-21. Access this article online Quick Response Code:
Reply to: Management of intraoperative hiccups with intravenous promethazine Sir, I read with pleasure the letters to the editor regarding my paper entitled “Persistent hiccups after lumbar epidural steroid injection,” which was published in your journal. The treatment of hiccups must be based on the etiology of the underlying disease. Treatment modalities may be classified as non-pharmacological, pharmacological and invasive methods. Non-pharmacological methods include holding one’s breath, drinking cold water, compression of the eyeball, carbon dioxide inhalation, nasogastric tube placement and gastric lavage.[1] The authors reported that they used some of these non-pharmacological methods in the intraoperative period; however, no benefit could be obtained. Pharmacological methods include metoclopramide, chlorpromazine, amitriptyline, phenytoin, valproic acid, baclofen and gabapentin, which are used as a monotherapy or combination therapy.[2] The authors reported that they treated hiccups that develop in the intraoperative period with a single dose of 12.5 mg promethazine. Although they reported that there was only one case report about promethazine use for the treatment of hiccups, they did not indicate any references.[3] It may be valuable for the treatment of hiccups, which develop in regional anesthesia and for a limited time during operations and which impair surgical comfort. We thank the author for their contribution. Serbülent Gökhan Beyaz Department of Anesthesiology and Reanimation, Sakarya University Medical School, Sakarya, Turkey Address for correspondence: Dr. Serbülent Gökhan Beyaz, Sakarya University Medical School, Department of Anesthesiology and Reanimation, Merkez Campus, Adnan Menderes Street, Adapazarı, Sakarya, Turkey. E-mail: [email protected] 114
Website: www.joacp.org
DOI: 10.4103/0970-9185.125724
Providing anesthesia in a remote location for radiation oncology in an adult Problems and solutions Sir, With the increasing role for anesthesiologists outside operating room locations, we are asked to provide services in unknown areas with limited resources. There is a significant mortality and morbidity associated with providing anesthesia in these locations.[1] We describe a patient successfully anesthetized in such a location (radiotherapy suite) on a daily basis for around 6 weeks. A 30-year-male (ASA III, weighing 90 kg) presented for radiation (photon beam) therapy, to treat invasive squamous cell carcinoma of the mastoid. Mild mental retardation due to cerebral palsy necessitated anesthesia to maintain immobility throughout the procedure. Although, the patient was able to understand verbal commands, he was unable to stay still for the duration of the procedure. His speech and language skills were fairly developed and communication skills were acceptable. Airway examination showed a Malampatti class 3 with adequate mouth opening and neck extension. The aims of anesthesia were to maintain spontaneous ventilation and immobility [Figure 1] without requiring significant airway intervention for the duration of the procedure. It was also important to ensure quick recovery facilitating early discharge as the procedure was planned only on an out-patient basis. After connecting to routine monitors and obtaining baseline
Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1
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.
