Karina Huerter practices in preventive, occupational, and primary care medicine at the Mayo Clinic, Rochester, Minnesota, and as needed in acute care at Olmsted Medical Center, also in Rochester.
No relationships to disclose.
A 62‐year‐old white female with a history of hyperlipidemia presented to the emergency department (ED) on a cold winter day with a chief complaint of bilateral ear pain and was triaged to urgent care (UC). In the absence of ear, nose, and throat pathology, the physician on duty recommended naproxen for pain relief. Two days later, the patient returned to UC with the same complaint of bilateral otalgia and was assigned to my care.
History The patient reported acute onset of bilateral ear pain 4 days prior, with no known triggers, such as trauma or recent upper respiratory tract infection. Pain had been persistent for the past 4 days and had not responded to treatment with naproxen. The patient described the pain as deep‐seated, constant, and steady and rated it as 5 on a 10‐point pain scale. She denied any ear discharge or fever. The pain was confined to both ears and did not radiate to the jaws or neck. Past medical history was significant for hyperlipidemia, treated with simvastatin (20 mg once daily), and lichen planus. Surgical history comprised cholecystectomy. She had no present or past history of tobacco smoking and did not drink alcohol.
Physical examination The patient was comfortable and in no acute distress. Vital signs were as follows: temperature, 98.4°F; heart rate, 86 beats per minute; respirations, 18 breaths per minute; BP, 165/81 mm Hg. Cardiac examination revealed a regular heart rate and rhythm with no murmurs or gallops. Lungs were clear to auscultation. Skin was warm, dry, and nondiaphoretic. Vascular examination revealed intact pulses in all four extremities, with no peripheral edema. Ear examination demonstrated intact tympanic membranes with good landmarks, no erythema, and no fluid bilaterally. The patient reported some ear discomfort during insertion of the otoscope.
>WHAT IS YOUR DIAGNOSIS?
* Trigeminal neuralgia
* Bronchogenic carcinoma
* Temporomandibular joint syndrome
The presence of known risk factors, such as hyperlipidemia and age, combined with incidental elevated high BP, raised the suspicion for acute coronary syndrome (ACS) in this patient despite a very atypical presentation. One clinical detail of the patient's symptomatology was crucial to cluing me in to the possibility that we might be dealing with ACS: The otalgia worsened whenever the patient was outdoors and exposed to frigid temperatures and improved in warmer environments.
Laboratory studies Blood work was significant for elevated cardiac biomarkers: a serum troponin I of 5.85 ng/mL (normal, <0.1 ng/mL) and a serum creatine kinase MB fraction (CK‐MB) of 27.1 ng/mL (reference range, 0.1‐6.3 ng/mL). Both were suggestive of ACS. Results of a CBC and electrolyte panel were within normal range. Compared with a normal ECG obtained as part of a pre‐anesthesia medical evaluation in 2001, a current ECG showed new T‐wave inversions and Q waves in the inferior and lateral leads. Based on these findings, which were consistent with an acute inferolateral non‐ST MI, the patient was transferred to an ED bed and connected to a heart monitor for closer surveillance of cardiac function. Additional blood work was obtained, including prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR). Since she had no contraindications, the patient was started on IV heparin per weight‐based protocol. She was given metoprolol 50 mg by mouth and sublingual nitroglycerin, which relieved her ear pain.
Treatment Within 2 hours of her arrival in UC, the patient was transported to a tertiary medical facility for advanced cardiac care, where she underwent cardiac catheterization. Coronary angiography showed a 90% obstruction of the proximal right coronary artery (RCA) with intracoronary thrombus. The patient underwent stenting of the RCA and thrombectomy.
Comment In a prospective study assessing referred cardiac symptomatology in 185 patients, Kreiner and colleagues concluded that only 6% of the study subjects exhibited craniofacial pain as the unique presentation for ischemia. Within this population, only 11 patients presented with bilateral otalgia and only two patients presented with unilateral ear pain.1 The proposed mechanism for craniofacial pain is explained by the connection between the vagus nerve and the trigeminal nerve nuclei.2 The vagus nerve is responsible for conducting pain perception to the external auditory meatus via the nerve of Arnold, which accounts for the ear pain experienced by some patients suffering ACS. The same principle applies to pain referred to the ear in the case of bronchogenic carcinoma, esophagitis, and aortic dissection.3
1. Kreiner M, Okeson JP, Michelis V, et al. Craniofacial pain as the sole symptom of cardiac ischemia: a prospective multicenter study. J Am Dent Assoc.
2. Rothwell PM. Angina and myocardial infarction presenting with pain confined to the ear. Postgrad Med J.
3. Bindoff LA, Heseltine D. Unilateral facial pain in patients with lung cancer: a referred pain via the vagus? Lancet.