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Loss of Smell and Taste After General Anesthesia: A Case Report

Baker, Jason Joe BSc; Öberg, Stina MD; Rosenberg, Jacob MD, DSc

doi: 10.1213/XAA.0000000000000612
Case Reports: Case Report

This case report describes a patient, who lost the ability to smell and taste after receiving a propofol-based general anesthesia for a laparoscopic inguinal hernia repair. Immediately after the procedure, the patient had anosmia (loss of smell), ageusia (loss of taste), and light dysphagia. Assessment by an otorhinolaryngologist and the results of a magnetic resonance imaging could not clarify the pathology behind these symptoms. Although there are several plausible explanations for the patient’s anosmia and ageusia (eg, cerebral infarcts, nerve damage, chronic sinusitis), the most likely explanation is an uncommon adverse drug reaction to the anesthetic agents used during the procedure.

From the Center for Perioperative Optimization, Department of Surgery, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.

Accepted for publication June 8, 2017

The authors declare no conflicts of interest.

Funding: None.

Address correspondence to Jason Joe Baker, BSc, Center for Perioperative Optimization, Department of Surgery, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark. Address e-mail to

General anesthesia is usually considered safe. However, there are reported cases of patients with distortion of taste and/or smell due to local anesthetics, stroke, nerve damage, or as a side effect of general anesthesia.1 We present a patient who developed anosmia (loss of smell) and ageusia (loss of taste) after undergoing an uneventful inguinal hernia repair under general anesthesia. The patient provided written consent for publication of the report.

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The 69-year-old male patient was scheduled for an elective laparoscopic inguinal hernia repair under general anesthesia. He was physically active, had a body mass index of 23 kg/m2, smoked 20 cigarettes a day, and took low-dose aspirin as secondary cardiovascular prevention because of hypertension.

Preoperatively, the patient received 1 g paracetamol, 400 mg ibuprofen, 8 mg dexamethasone, 4 mg ondansetron, and subcutaneous unfractionated heparin. General anesthesia was induced and maintained by a total of 530 mg propofol and 2.15 mg remifentanil, and no muscle relaxants were administered. Endotracheal intubation was difficult and 3 attempts were necessary to establish an airway. After intubation, the lungs were ventilated with a mixture of oxygen and air, and 260 mL of Ringer’s acetate solution was administered intraoperatively. The intraoperative course was uneventful and fentanyl 0.1 mg was administered before uncomplicated tracheal extubation. The duration of the surgery was 30 minutes. On the first postoperative day, the patient complained about anosmia, ageusia, an irritated throat, and light dysphagia. The patient treated the dysphagia by drinking water when swallowing food. The patient reported normal smell and taste before the operation. The patient was discharged with these symptoms and advised to contact the hospital if they persisted.

Information of the patient’s medical and family history was obtained preoperatively. The patient’s brother and 2 nephews have pseudocholinesterase deficiency, which the patient had not been tested for. He had also previously been operated under general anesthesia without any postoperative complications.

Five weeks later, the patient reported a similar constellation of symptoms as when he was discharged, and contacted the hospital for further instructions. The timeline from the operation to the last follow-up is shown in the Figure. Two and a half months postoperatively, an otorhinolaryngologist examined the patient. Indirect laryngoscopy by fibroscopy revealed a normal rhinopharynx, hypopharynx, and larynx. There were no signs of pus, fungal infection, or mucosal changes. The otorhinolaryngologist referred the patient to a magnetic resonance imaging (MRI) of the cerebrum with a focus on the anterior fossa and olfactory region. He was instructed to use a nasal spray containing antihistamine and glucocorticoid as a diagnostic measure to exclude allergic rhinitis.



Seven months after the operation, the patient had an MRI. The MRI findings showed no signs of hydrocephalus, tumors, or bleeding. There were normal conditions in the cerebellum, the brainstem, and in the anterior fossa. There were slight abnormalities on the scan, including a centered ventricular system with possible calcifications of the choroid plexus, small changes of the periventricular system probably due to cerebral microangiopathy, signs of moderate cortical atrophy, and thickened mucosal layers in the ethmoidal, maxillary, and sphenoid sinuses. However, these abnormal findings could not explain the simultaneous loss of both smell and taste. A second MRI with contrast would have been preferable; however, this was precluded because of the patient’s claustrophobia.

One year after the operation, the patient was visited for further anamnestic information. He denied being able to taste sweet, sour, bitter, or salt, and also denied being able to smell any odors. He continued to drink water during meals to assist with swallowing. Subsequently, 1 month later, he was able to smell strong perfumes.

The patient’s senses were tested 16 months after the operation. He was not able to recognize sweet, sour, bitter, or salt. The smell was tested once with 12 different odors, and for each odor, the patient had to choose among 4 answers. He was exposed to odors of orange, leather, cinnamon, mint, banana, lemon, liquorish, coffee, clove, pineapple, rose, and fish. He answered correctly for 10 of 12 odors and selected the wrong answer for cinnamon and banana.

There have not been any therapeutic interventions besides the nasal spray, which was ineffective. The patient reported severely impaired quality of life because of this condition.

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The patient’s symptoms could be explained by a single or several factors occurring simultaneously. The anosmia may be due to chronic sinusitis, which the MRI showed signs of, or age-related anosmia. Mucosal inflammation contributes to a decrease of the olfactory function, and patients with chronic sinusitis have a higher degree of erosion of the olfactory epithelium compared with controls.2 However, these pathologies are slowly evolving and do not explain the sudden loss of smell, unless it was lost before the operation and only detected afterward because of simultaneous loss of taste.

The anosmia could also be explained by an infarct in the olfactory pathway too small to see on an MRI without contrast, but this would unlikely have caused the ageusia. Taste and smell are usually perceived as one experience, but a study testing the ability of tasting in 600 patients with smell dysfunction concluded that anosmia did not seem to affect the taste.3 Therefore, damage solely to the olfactory pathway is unlikely to explain the simultaneous ageusia.

A small infarct along the gustatory pathway would explain the ageusia. In another case report, a patient had a unilateral infarct in the thalamus causing bilateral ageusia without affecting other cranial nerves.4 The thalamus receives both taste and smell projections. The olfactory pathway primarily sends projections directly to the cortex and only sends secondary projections through the thalamus, whereas the gustatory projections are mainly sent through the thalamus before reaching the cortex.5 This suggests that an infarct in the thalamus might explain the ageusia and a dysfunction of the smell. In our case, chronic sinusitis might have contributed to further impairment of the smell.

The ageusia could also be caused by peripheral nerve damage. This scenario would require damage to both lingual nerves and lingual branches of the glossopharyngeal nerves. The lingual nerves carry both gustatory and sensory fibers.5 The vagus nerves receive information from a limited area and would not lead to ageusia if damaged. A previous case report presented a patient with taste dysfunction on the anterior two-thirds of the tongue and an intact sensory function, after receiving a general anesthetic with a laryngeal mask airway.6 The authors hypothesized that the pressure from the laryngeal mask had caused damage to the lingual nerves. Similarly, our patient had a sore throat and light dysphagia postoperatively, most likely as a result of the repeated attempts at intubation. The etiology to the selective damage to the taste fibers is unknown.

Because of the suddenness, it is unlikely that the symptoms are caused by cerebral microangiopathy and cortical atrophy. Even though the patient did not receive succinylcholine, he did receive other drugs. Pseudocholinesterase deficiency could be related to sensitivity to other drugs,7 and it is unclear if the patient suffers from this deficiency. However, the patient had previously undergone general anesthesia without complications, although it is unknown which anesthetics he received. If the symptoms were caused by the anesthetic medication, it could explain the sudden and simultaneous loss. Several drugs are suspected of causing ageusia and anosmia8,9; however, the frequency of these disturbances caused by general anesthesia is unclear, and may only be resolved by awareness of such cases.10 Furthermore, these effects are usually temporary8,9 and in fact, the patient did regain some of his ability to smell after 1 year. Anesthetic drugs may affect the central and/or peripheral nervous system, the mucus secretion, or damage the olfactory and gustatory neuroepithelium.8 Propofol stimulates the inhibitory γ-aminobutyric acid type A receptors in the central nervous system.11 These receptors inhibit the gustatory and olfactory pathways. In experimental animal studies, propofol disrupted the olfactory and the gustatory memories12,13 and the postoperative ability to recognize odors that were administered during the anesthesia.14 The inhibitory effect of propofol on the olfactory system was greater than that of fentanyl.12 These findings suggest that propofol has the potential of inhibiting the olfactory and gustatory pathways.

The strengths of this case report were the tests of the senses and the access to the patient’s records, which combined with the immediate anosmia and ageusia, minimized the risk of recall bias. However, there is a small risk of recall bias regarding the preoperative status, but the patient denied having impaired senses before the operation. The lack of a computed tomography scan and an MRI with contrast is a limitation. These scans could have ruled out sinusitis and small brain infarcts.

In conclusion, simultaneous ageusia and anosmia after general anesthesia suggests a drug-induced reaction. Contributing factors could be a traumatic intubation damaging the lingual nerves or an undetected infarct in the thalamus. The MRI showed signs of sinusitis, but the patient reported a normal smell before the operation. The overall evidence suggests that the anesthetic drugs caused the postoperative ageusia and anosmia.

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Name: Jason Joe Baker, BSc.

Contribution: This author helped acquire and interpret the data, and draft the manuscript.

Name: Stina Öberg, MD.

Contribution: This author helped interpret the data, and revise the manuscript.

Name: Jacob Rosenberg, MD, DSc.

Contribution: This author helped conceive and design the study, and revise the manuscript.

This manuscript was handled by: Hans-Joachim Priebe, MD, FRCA, FCAI.

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