A 76-year-old man (height, 154 cm; weight, 53 kg) presented with a 3-month history of left shoulder pain. His pain persisted despite conservative treatment. Magnetic resonance imaging was performed to determine its exact cause and revealed full-thickness tears of the supraspinatus and infraspinatus tendons (Fig. 1). The patient was scheduled to undergo arthroscopic rotator cuff repair under general anesthesia.

Given his age, the patient’s physical status was classified as American Society of Anesthesiologists class II, despite him being a non-smoker with no history of alcohol consumption. His medical history included dyslipidemia, and there was no known history of allergies. The preoperative laboratory findings showed a white blood cell (WBC) count of 6.0×10³/µL (normal, 4.0–10.0×10³/µL) and C-reactive protein (CRP) level of 0.05 mg/dL (normal, 0–0.5 mg/dL). The patient was initially placed in a supine position, and general anesthesia was induced using propofol (2 mg/kg) and fentanyl (2 µg/kg). Endotracheal intubation (internal diameter, 7.5 mm) was performed after muscle relaxation with rocuronium (1 mg/kg), and sevoflurane (1 minimum alveolar concentration) was used for maintenance of anesthesia.

The patient was carefully placed in the right lateral decubitus position with the left side facing up. The operated left arm was pulled into a 30° abduction and 20° forward flexion position with a weight of approximately 10 pounds, using a traction device (Fig. 2). Appropriate padding was used to support the right side of the patient’s head, and an axillary roll was used to protect the brachial plexus of the right shoulder. All bony prominences and neurovascular structures were carefully padded. The applied pressure of the irrigation pumping system for arthroscopic surgery was set at 30 mmHg. The arthroscopic findings were a rotator cuff tear with a mediolateral measurement of 3.0 cm and an anteroposterior measurement of 2.5 cm (Fig. 3A). Rotator cuff repair was performed using the double-row suture bridge technique with 2 medial suture anchors (Healix Advance BR; Depuy Mitek) and 2 lateral anchors (ReelX STT; Stryker) with 5 mattress sutures (Fig. 3B). The surgery lasted approximately 110 minutes and was uneventful. At the end of the procedure, the patient was placed in the supine position, anesthesia was reversed with an injection of glycopyrrolate (0.4 mg) and pyridostigmine bromide (15 mg), and the patient was extubated.

The morning after surgery, the patient complained of left facial swelling (Fig. 4A). A physical examination revealed swelling of the left cheek around the parotid gland. There was no pain, redness, crepitus, or any other sign or symptom of inflammation. Previous neck masses, salivary calculus, and inflammation were differential diagnoses, but the patient had no history of a parotid or neck mass or salivary calculus and had neither autoimmune disease nor fever. As swelling gradually increased, we requested an ear, nose, and throat (ENT) consultation. On enhanced computed tomography scan performed based on ENT recommendations, we determined that the left parotid gland associated with the adjacent subcutaneous soft tissue was enlarged (Fig. 4B). Salivary calculus and ductal dilatation were not observed, but level II lymphadenopathy was present. Laryngoscopy confirmed the absence of redness or swelling of the nasopharynx, oropharynx, laryngopharynx, or epiglottis, and no airway obstruction was observed. The laboratory findings indicated that the patient’s WBC count was increased by 12.9 ×10³/µL and the CRP level by 5.46 mg/dL. In addition, amylase level, which increases during parotitis, was elevated to 2,433 U/L (normal, 40–140 U/L). Based on these findings, the patient was diagnosed with acute postoperative transient parotitis.

We treated the patient with 3 g of intravenous ampicillin/sulbactam every 6 hours. The WBC count and CRP level decreased to 8.5×10³/µL and 5.25 mg/dL, respectively, on postoperative day 3 and further decreased to 6.8×10³/µL and 2.75 mg/µL on postoperative day 4. Ultimately, the parotid swelling subsided 6 days postoperatively. The patient was discharged with a prescription of cefditoren, a third-generation oral cephalosporin, for 2 weeks. After the patient’s symptoms resolved, no other special treatment was needed, and there was no recurrence as of one year after surgery.

Acute postoperative parotitis observed after general anesthesia is commonly referred to as “anesthesia mumps [2].” It was first described as “surgical mumps” by Schwarz et al. in the 1960s and defined as “anesthesia mumps” by Reilly et al. 10 years later when they reported three patients with transient swelling of the parotid glands among approximately 1,500 patients who underwent general anesthesia [2]. Since then, acute postoperative parotitis after general anesthesia has been commonly referred to as “anesthetic mumps” [2] and has an incidence rate of 0.16%–0.2% [2]. The complication is often reported in case studies in various fields, including neurosurgery, general surgery, plastic surgery, orthopedic surgery, and gynecology [2]. When comparing our case to other documented cases of acute postoperative parotitis, the timing of symptom onset was similar, but the only symptom observed was swelling.

Several reports have suggested possible etiological factors underlying acute postoperative parotitis [7,8]. Among these, three cases were associated with the use of general anesthesia [8]. First, when positive pressure mask ventilation is applied to the mouth, air can retrograde to the parotid glands and cause pneumo-parotitis. Second, drugs such as atropine, succinylcholine, morphine, and inhalational anesthetics can cause salivary gland obstruction by reducing salivary secretion in patients with insufficient hydration [8,9]. Third, excessive stress, such as coughing or sneezing during extubation, can block the salivary canal [8]. In our case report, general anesthesia was performed; thus, there is a possibility that the parotitis was caused by the 3 aforementioned causes related to general anesthesia.

Another possible etiological factor is related to the surgical position. When a prone or lateral decubitus position is required during surgery, the parotid gland on the side of the head may be compressed if the head is pressed or excessively rotated [2,8]. In particular, this position is more likely to cause ischemic parotitis in obese patients with short and thick necks in the supine or lateral positions by compressing blood vessels and interfering with perfusion of the area supplied [2,5]. In previous case studies, most patients who underwent surgery in the lateral decubitus position experienced swelling on the side of their face that was pressed [2,5,8]. However, in our case report, the patient developed parotitis on the opposite side of his face. This indicates that adequate padding was applied to prevent compression during surgery. The cause of parotitis on the same side was assumed to be excessive tension and strain on the neck caused by pulling the operated arm with a weight of approximately 10 pounds. Furthermore, extraarticular fluid leakage used for continuous irrigation of the joint space was absorbed into the subcutaneous soft tissue around the neck [10]. The lateral position may also contribute to the movement of subcutaneous fluid from the shoulder to the neck by gravity [10]. Excessive shear stress or compression of blood vessels may cause venous congestion or arterial ischemia around the neck, which can lead to postoperative parotitis [10].

According to previous case reports, most cases of postoperative parotitis resolve spontaneously within 1 week [8]. Multiple etiological factors can cause postoperative parotitis, but the treatment is usually similar regardless of cause. Adequate hydration and pain control through the administration of anti-inflammatory medications such as non-steroidal anti-inflammatory drugs, mouthwash, and warm compress applications can help relieve symptoms [7]. Medical treatments such as oral or intravenous antibiotics can prevent secondary bacterial infections [7]. However, a few cases of airway obstruction that required reintubation have been reported [2,3]. Therefore, caution is recommended when removing the endotracheal tube after surgery in patients with rapidly progressing postoperative parotitis. In our case, the parotitis subsided 6 days after surgery. Following ENT recommendations, 3 g of ampicillin/sulbactam was intravenously injected every 6 hours and oral antibiotics were administered for 2 weeks prior to discharge. Therefore, it is important to promptly request an ENT consultation if necessary and avoid delay in diagnosis and treatment.

To the best of our knowledge, this is the first reported case of acute transient parotitis following arthroscopic repair of the rotator cuff. It is also important to remain aware of cases of acute transient parotitis because symptoms can range from mild to life-threatening airway obstruction. Anesthesiologists and orthopedic surgeons should pay attention to the insertion and removal of the endotracheal tube and the surgical position of the patient. When positioning the patient, surgeons should apply appropriate padding to prevent compression of the parotid gland and duct and be careful not to overstress the patient's head and neck. Additionally, it is important not to overapply traction and to explain to patients in advance that traction may cause facial swelling. To avoid panic regarding acute postoperative parotitis, surgeons must be aware of rare complications and should closely monitor patients postoperatively. Early diagnosis and prompt treatment are also critical to improving patient outcomes. If necessary, it is important to promptly request ENT consultation to ensure timely diagnosis and treatment.