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Anosmia and hypogeusia as a complication of general anesthesia
Journal of Clinical Anesthesia (2012) 24, 231–233
Case Report
Anosmia and hypogeusia as a complication of general anesthesia Nadya M. Dhanani MD (Resident), Yandong Jiang MD, PhD (Assistant Professor)⁎ Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA Received 22 September 2010; revised 15 August 2011; accepted 27 August 2011
Keywords: Anesthesia; General: complications; Anosmia; Hypogeusia
Abstract A 57 year old woman with no previous history of any sensory deficits developed anosmia and hypogeusia after general anesthesia for laparoscopic cholecystectomy, with complete recovery over 6 months. There were no other identifiable factors that may have contributed to her anosmia and hypogeusia after general anesthesia. As anosmia and hypogeusia related to anesthesia and surgery are not frequently reported, the incidence of these events related to anesthesia may be higher than expected. © 2012 Elsevier Inc. All rights reserved.
1. Introduction While inhalational and intravenous anesthetics are considered safe and relatively well tolerated by many patients, there are side effects of these pharmacologic agents. Alterations in smell and/or taste are not frequently reported complications of general anesthesia. Harris et al reported in a retrospective study of patients who underwent upper gastrointestinal surgery, that almost half of the patients presented postoperatively with a transient loss of taste and/or smell [1]. Henkin reported that approximately 4% of the patients with taste and/or smell dysfunction had recently undergone general anesthesia [2]. The exact incidence of this complication remains unknown and seems higher than expected. It is likely that a majority of patients who experience a diminished and/or loss of taste and smell after general anesthesia report this event to other physicians rather than their anesthesia care providers. ⁎ Correspondence: Yandong Jiang, MD, PhD, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, 55 Fruit St., Jackson 422, Boston, MA 02114, USA. Tel.: +1 617 724-2366; fax: +1 617 724-8500. E-mail address: [email protected] (Y. Jiang). 0952-8180/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2011.08.005
Therefore, both the incidence and significance of this complication are under-appreciated. A case of transient anosmia (complete loss of smell) and hypogeusia (diminished sense of taste) following abdominal surgery during inhalational general anesthesia is presented.
2. Case report A 57 year old woman was diagnosed with cholecystitis and scheduled for an elective laparoscopic cholecystectomy. The patient had a past medical history significant for depression, migraine headaches, and acute sinusitis. Of note, the patient denied any aura or neurologic symptoms associated with her migraine headaches, and she also denied any loss of smell with her episodes of acute sinusitis in the past. Her medication regimen before surgery included fluoxetine, sumatriptan, aspirin, calcium/vitamin D, vitamin C, gingko biloba, and a multivitamin. The patient reported an allergy to oxycodone, which had caused an anaphylactic reaction in the past. Her surgical history was pertinent for the removal of an ovarian cyst during general anesthesia in 1974, followed by the removal of ovarian scar tissue using
232 neuraxial anesthesia a few years later. Her anesthetic history was notable for postoperative nausea and vomiting (PONV) after her general anesthetic 34 years ago. There was no family history of adverse events with anesthesia, taste or smell dysfunction, or neurologic disorders. On the day of surgery, the patient was given 2.0 mg of midazolam preoperatively. She received 250 μg of fentanyl, 150 mg of propofol, and 50 mg of rocuronium for induction and tracheal intubation. After intubation with an endotracheal tube, anesthesia was maintained with sevoflurane (2.5%), an oxygen/air mixture, and propofol infusion (25 μg/kg/min). The patient was given 10 mg of morphine for postoperative analgesia. She received a 1.5 mg transdermal scopolamine patch and 8 mg of dexamethasone and 4 mg of ondansetron for PONV prophylaxis. An orogastric tube was placed for the duration of the procedure. The patient remained hemodynamically stable intraoperatively and the surgery was completed uneventfully. The patient's trachea was extubated, and she recovered in the Postanesthesia Care Unit. She was monitored on the hospital floor overnight and discharged home the following day. The patient's initial postoperative recovery was unremarkable. Once home, she tolerated a regular diet, had adequate pain control with oral analgesics, and performed her activities of daily living without difficulty. Two weeks after surgery, she noticed that her sense of smell was lost. She realized that she was unable to smell a variety of scents, including flowers, household pets, and certain foods. The patient also reported a decreased ability to discern flavor from food. However, this deficit was incomplete. She denied any qualitative distortions of taste or smell, and reported only diminished sensations of both. There were no signs of sinusitis (nasal congestion or discharge). She denied any other associated symptoms such as headaches, tinnitus, loss of hearing, or visual disturbances during this time. Ultimately, although there was no formal evaluation or therapy directed at her condition, she gradually regained full sense of both smell and taste and reported complete recovery 6 months after the surgery. To help determine the extent and time course of the primary sensory deficit, anosmia, we used the visual analog scale (VAS), with 0 = complete loss of smell and 100 = intact sense of smell. The patient reported a VAS score of 0 when she initially noticed the loss of smell. She noted that her sense of smell improved to a VAS score of 10 at three months, a VAS score of 20 at 4 months, and a VAS score of 100 at 6 months with complete resolution.
3. Discussion Anatomically, perception of smell is mediated by olfactory receptors in the nose, olfactory nerves, olfactory bulbs, and several regions of the brain. While nasal pathology such as nasal polyps, sinusitis, and nasal tumors are well known to affect the sense of smell, data attributing
N.M. Dhanani, Y. Jiang the loss of smell to general anesthesia remain scant [3]. General anesthesia suppresses the neuronal signal conduction at various levels of all the sensory pathways, including at the receptor, axon, neurosynapse, and cortex [4,5]. Such an effect on sensory pathways has been shown with somatosensory-evoked potentials, visual-evoked potentials, and auditory-evoked potentials; the effect is transient and completely reversible [6-8]. However, the effects of general anesthesia on the sense of smell and taste, and the time courses of their recovery, remain to be determined. Konstantinidis et al reported a 60 year old woman who had a 3-month history of altered smell after general anesthesia with propofol and sevoflurane for a urologic operation [9]. In their report, the authors offered scientific support for their hypotheses linking inhalational and intravenous anesthetics to dysosmia (a distorted identification of smell). They cited clinical studies that have shown that sevoflurane and propofol affect γ-aminobutyric acid (GABA) receptor ligand binding [10]. Given that GABA is the main inhibitory neurotransmitter of the brain involved in many areas, including synapses in olfactory bulbs, it is conceivable that such anesthetic agents may affect the olfactory system at any level of the pathway [9,11]. In fact, decreased brain GABA has been seen in patients with phantageusia and phantosmia (olfactory and gustatory hallucination, respectively), with clinical improvement after an increase in brain GABA levels by GABAergic drugs [11]. Both propofol and fentanyl decrease the olfactory response of rats after infusion, with propofol having the most significant effect [12]. In 1972, Nicoll studied the effects of anesthetics such as halothane and pentobarbitone on the extracellular field potentials of the olfactory bulb [13]. The author found that large doses of anesthetics depressed the synaptic excitation of granule cells and prolonged the post-synaptic inhibition of mitral cells involved in the lateral olfactory tract of rabbits [13]. Although we were unable to obtain imaging to rule out intracranial or nasal pathology in our patient, we believe that the loss of smell was unlikely due to mechanical injury. She did not have a nasogastric tube placed, and the loss of smell was not accompanied by any other neurological deficits. In addition, the patient's recovery was gradual and it was completed without any medical intervention. Functional magnetic resonance imaging of the brain (fMRI) may help to identify the location of the neurologic insult, peripheral versus central, and the time course of recovery at each potentially affected site. Since the olfactory system is considered a primal sensory function, the speed of its recovery postoperatively may serve as a broader indicator of recovery from general anesthesia. Elucidating the complicated relationship between general anesthesia and the olfactory and gustatory systems requires further investigation with well-designed controlled studies. Understanding the mechanism of association between alterations in the sensation of smell, taste, and anesthesia
Anosmia, hypogeusia, and general anesthesia may help us to redefine “recovery from anesthesia” and improve the quality of patient care in the future.
References [1] Harris AM, Griffin SM. Postoperative taste and smell deficit after upper gastrointestinal cancer surgery – an unreported complication. J Surg Oncol 2003;82:147-50. [2] Henkin RI. Altered taste and smell after anesthesia: cause and effect? Reply. Anesthesiology 1995;83:648-9. [3] Henkin RI. Drug induced taste and smell disorders. Incidence, mechanisms and management related primarily to treatment of sensory receptor dysfunction. Drug Saf 1994;11:318-77. [4] Antkowiak B, Kirschfeld K. Neural mechanisms of anesthesia. Anasthesiol Intensivmed Notfallmed Schmerzther 2000;35:731-43. [5] Campagna JA, Miller KW, Forman SA. Mechanisms of actions of inhaled anesthetics. N Engl J Med 2003;348:2110-24. [6] Thiel A, Russ W, Hempelmann G. Evoked potentials and inhalational anesthetics. Klin Wochenschr 1998;66(Suppl 14):11-8.
233 [7] Hudetz AG, Vizuete JA, Imas OA. Desflurane selectively suppresses long-latency cortical neuronal response to flash in the rat. Anesthesiology 2009;111:231-9. [8] Sebel PS, Ingram DA, Flynn PJ, Rutherfoord CF, Rogers H. Evoked potentials during isoflurane anaesthesia. Br J Anaesth 1986;58: 580-5. [9] Konstantinidis I, Tsakiropoulou E, Iakovou I, Douvantzi A, Metaxas S. Anosmia after general anaesthesia: a case report. Anaesthesia 2009;64:1367-70. [10] Salmi E, Kaisti KK, Metsãhonkala L, et al. Sevoflurane and propofol increase 11C-flumazenil binding to gamma-aminobutyric acidA receptors in humans. Anesth Analg 2004;99:1420-6. [11] Levy LM, Henkin RI. Brain gamma-aminobutyric acid levels are decreased in patients with phantageusia and phantosmia demonstrated by magnetic resonance spectroscopy. J Comput Assist Tomogr 2004;28:721-7. [12] Jugovac I, Imas O, Hudetz AG. Supraspinal anesthesia: behavioral and electroencephalographic effects of intracerebroventricularly infused pentobarbital, propofol, fentanyl, and midazolam. Anesthesiology 2006;105:764-78. [13] Nicoll RA. The effects of anaesthetics on synaptic excitation and inhibition in the olfactory bulb. J Physiol 1972;223:803-14.
Case Report
Anosmia and hypogeusia as a complication of general anesthesia Nadya M. Dhanani MD (Resident), Yandong Jiang MD, PhD (Assistant Professor)⁎ Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114, USA Received 22 September 2010; revised 15 August 2011; accepted 27 August 2011
Keywords: Anesthesia; General: complications; Anosmia; Hypogeusia
Abstract A 57 year old woman with no previous history of any sensory deficits developed anosmia and hypogeusia after general anesthesia for laparoscopic cholecystectomy, with complete recovery over 6 months. There were no other identifiable factors that may have contributed to her anosmia and hypogeusia after general anesthesia. As anosmia and hypogeusia related to anesthesia and surgery are not frequently reported, the incidence of these events related to anesthesia may be higher than expected. © 2012 Elsevier Inc. All rights reserved.
1. Introduction While inhalational and intravenous anesthetics are considered safe and relatively well tolerated by many patients, there are side effects of these pharmacologic agents. Alterations in smell and/or taste are not frequently reported complications of general anesthesia. Harris et al reported in a retrospective study of patients who underwent upper gastrointestinal surgery, that almost half of the patients presented postoperatively with a transient loss of taste and/or smell [1]. Henkin reported that approximately 4% of the patients with taste and/or smell dysfunction had recently undergone general anesthesia [2]. The exact incidence of this complication remains unknown and seems higher than expected. It is likely that a majority of patients who experience a diminished and/or loss of taste and smell after general anesthesia report this event to other physicians rather than their anesthesia care providers. ⁎ Correspondence: Yandong Jiang, MD, PhD, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, 55 Fruit St., Jackson 422, Boston, MA 02114, USA. Tel.: +1 617 724-2366; fax: +1 617 724-8500. E-mail address: [email protected] (Y. Jiang). 0952-8180/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2011.08.005
Therefore, both the incidence and significance of this complication are under-appreciated. A case of transient anosmia (complete loss of smell) and hypogeusia (diminished sense of taste) following abdominal surgery during inhalational general anesthesia is presented.
2. Case report A 57 year old woman was diagnosed with cholecystitis and scheduled for an elective laparoscopic cholecystectomy. The patient had a past medical history significant for depression, migraine headaches, and acute sinusitis. Of note, the patient denied any aura or neurologic symptoms associated with her migraine headaches, and she also denied any loss of smell with her episodes of acute sinusitis in the past. Her medication regimen before surgery included fluoxetine, sumatriptan, aspirin, calcium/vitamin D, vitamin C, gingko biloba, and a multivitamin. The patient reported an allergy to oxycodone, which had caused an anaphylactic reaction in the past. Her surgical history was pertinent for the removal of an ovarian cyst during general anesthesia in 1974, followed by the removal of ovarian scar tissue using
232 neuraxial anesthesia a few years later. Her anesthetic history was notable for postoperative nausea and vomiting (PONV) after her general anesthetic 34 years ago. There was no family history of adverse events with anesthesia, taste or smell dysfunction, or neurologic disorders. On the day of surgery, the patient was given 2.0 mg of midazolam preoperatively. She received 250 μg of fentanyl, 150 mg of propofol, and 50 mg of rocuronium for induction and tracheal intubation. After intubation with an endotracheal tube, anesthesia was maintained with sevoflurane (2.5%), an oxygen/air mixture, and propofol infusion (25 μg/kg/min). The patient was given 10 mg of morphine for postoperative analgesia. She received a 1.5 mg transdermal scopolamine patch and 8 mg of dexamethasone and 4 mg of ondansetron for PONV prophylaxis. An orogastric tube was placed for the duration of the procedure. The patient remained hemodynamically stable intraoperatively and the surgery was completed uneventfully. The patient's trachea was extubated, and she recovered in the Postanesthesia Care Unit. She was monitored on the hospital floor overnight and discharged home the following day. The patient's initial postoperative recovery was unremarkable. Once home, she tolerated a regular diet, had adequate pain control with oral analgesics, and performed her activities of daily living without difficulty. Two weeks after surgery, she noticed that her sense of smell was lost. She realized that she was unable to smell a variety of scents, including flowers, household pets, and certain foods. The patient also reported a decreased ability to discern flavor from food. However, this deficit was incomplete. She denied any qualitative distortions of taste or smell, and reported only diminished sensations of both. There were no signs of sinusitis (nasal congestion or discharge). She denied any other associated symptoms such as headaches, tinnitus, loss of hearing, or visual disturbances during this time. Ultimately, although there was no formal evaluation or therapy directed at her condition, she gradually regained full sense of both smell and taste and reported complete recovery 6 months after the surgery. To help determine the extent and time course of the primary sensory deficit, anosmia, we used the visual analog scale (VAS), with 0 = complete loss of smell and 100 = intact sense of smell. The patient reported a VAS score of 0 when she initially noticed the loss of smell. She noted that her sense of smell improved to a VAS score of 10 at three months, a VAS score of 20 at 4 months, and a VAS score of 100 at 6 months with complete resolution.
3. Discussion Anatomically, perception of smell is mediated by olfactory receptors in the nose, olfactory nerves, olfactory bulbs, and several regions of the brain. While nasal pathology such as nasal polyps, sinusitis, and nasal tumors are well known to affect the sense of smell, data attributing
N.M. Dhanani, Y. Jiang the loss of smell to general anesthesia remain scant [3]. General anesthesia suppresses the neuronal signal conduction at various levels of all the sensory pathways, including at the receptor, axon, neurosynapse, and cortex [4,5]. Such an effect on sensory pathways has been shown with somatosensory-evoked potentials, visual-evoked potentials, and auditory-evoked potentials; the effect is transient and completely reversible [6-8]. However, the effects of general anesthesia on the sense of smell and taste, and the time courses of their recovery, remain to be determined. Konstantinidis et al reported a 60 year old woman who had a 3-month history of altered smell after general anesthesia with propofol and sevoflurane for a urologic operation [9]. In their report, the authors offered scientific support for their hypotheses linking inhalational and intravenous anesthetics to dysosmia (a distorted identification of smell). They cited clinical studies that have shown that sevoflurane and propofol affect γ-aminobutyric acid (GABA) receptor ligand binding [10]. Given that GABA is the main inhibitory neurotransmitter of the brain involved in many areas, including synapses in olfactory bulbs, it is conceivable that such anesthetic agents may affect the olfactory system at any level of the pathway [9,11]. In fact, decreased brain GABA has been seen in patients with phantageusia and phantosmia (olfactory and gustatory hallucination, respectively), with clinical improvement after an increase in brain GABA levels by GABAergic drugs [11]. Both propofol and fentanyl decrease the olfactory response of rats after infusion, with propofol having the most significant effect [12]. In 1972, Nicoll studied the effects of anesthetics such as halothane and pentobarbitone on the extracellular field potentials of the olfactory bulb [13]. The author found that large doses of anesthetics depressed the synaptic excitation of granule cells and prolonged the post-synaptic inhibition of mitral cells involved in the lateral olfactory tract of rabbits [13]. Although we were unable to obtain imaging to rule out intracranial or nasal pathology in our patient, we believe that the loss of smell was unlikely due to mechanical injury. She did not have a nasogastric tube placed, and the loss of smell was not accompanied by any other neurological deficits. In addition, the patient's recovery was gradual and it was completed without any medical intervention. Functional magnetic resonance imaging of the brain (fMRI) may help to identify the location of the neurologic insult, peripheral versus central, and the time course of recovery at each potentially affected site. Since the olfactory system is considered a primal sensory function, the speed of its recovery postoperatively may serve as a broader indicator of recovery from general anesthesia. Elucidating the complicated relationship between general anesthesia and the olfactory and gustatory systems requires further investigation with well-designed controlled studies. Understanding the mechanism of association between alterations in the sensation of smell, taste, and anesthesia
Anosmia, hypogeusia, and general anesthesia may help us to redefine “recovery from anesthesia” and improve the quality of patient care in the future.
References [1] Harris AM, Griffin SM. Postoperative taste and smell deficit after upper gastrointestinal cancer surgery – an unreported complication. J Surg Oncol 2003;82:147-50. [2] Henkin RI. Altered taste and smell after anesthesia: cause and effect? Reply. Anesthesiology 1995;83:648-9. [3] Henkin RI. Drug induced taste and smell disorders. Incidence, mechanisms and management related primarily to treatment of sensory receptor dysfunction. Drug Saf 1994;11:318-77. [4] Antkowiak B, Kirschfeld K. Neural mechanisms of anesthesia. Anasthesiol Intensivmed Notfallmed Schmerzther 2000;35:731-43. [5] Campagna JA, Miller KW, Forman SA. Mechanisms of actions of inhaled anesthetics. N Engl J Med 2003;348:2110-24. [6] Thiel A, Russ W, Hempelmann G. Evoked potentials and inhalational anesthetics. Klin Wochenschr 1998;66(Suppl 14):11-8.
233 [7] Hudetz AG, Vizuete JA, Imas OA. Desflurane selectively suppresses long-latency cortical neuronal response to flash in the rat. Anesthesiology 2009;111:231-9. [8] Sebel PS, Ingram DA, Flynn PJ, Rutherfoord CF, Rogers H. Evoked potentials during isoflurane anaesthesia. Br J Anaesth 1986;58: 580-5. [9] Konstantinidis I, Tsakiropoulou E, Iakovou I, Douvantzi A, Metaxas S. Anosmia after general anaesthesia: a case report. Anaesthesia 2009;64:1367-70. [10] Salmi E, Kaisti KK, Metsãhonkala L, et al. Sevoflurane and propofol increase 11C-flumazenil binding to gamma-aminobutyric acidA receptors in humans. Anesth Analg 2004;99:1420-6. [11] Levy LM, Henkin RI. Brain gamma-aminobutyric acid levels are decreased in patients with phantageusia and phantosmia demonstrated by magnetic resonance spectroscopy. J Comput Assist Tomogr 2004;28:721-7. [12] Jugovac I, Imas O, Hudetz AG. Supraspinal anesthesia: behavioral and electroencephalographic effects of intracerebroventricularly infused pentobarbital, propofol, fentanyl, and midazolam. Anesthesiology 2006;105:764-78. [13] Nicoll RA. The effects of anaesthetics on synaptic excitation and inhibition in the olfactory bulb. J Physiol 1972;223:803-14.