A case of Stanford B type aortic dissection in a patient whose initial complaints were a toothache and left shoulder pain

Dear Editor,

A 49-year-old male experienced an abnormal sound with a toothache and left shoulder pain during sleep. His chief complaint was lumbago at rest, and he had a history of untreated hypertension. The results of a physical examination were negative. Upon arrival, he was conscious with a blood pressure of 184/100 mmHg without significant laterality. A chest roentgen revealed protrusion of the left first and an increase in the cardiothoracic ratio to over 50%. A serum biochemical analysis demonstrated fibrinogen degradation product level of 64.2 μg/ml and negative findings for troponin T. An electrocardiogram showed sinus tachycardia, while cardiac sonography was negative. Although plain CT showed no abnormalities, enhanced CT disclosed Stanford B type aortic dissection from the aortic arch to the bifurcation of the common iliac artery [Figure 1]. A diagnosis of aortic dissection was made within 20 minutes of the patient's arrival. As he did not present with any signs of organ ischemia, conservative therapy to control blood pressure and pain using a β-blocker and fentanyl was selected, and he was discharged on the 15^th hospital day.

Figure 1.

Enhanced CT performed on arrival The CT scan shows Stanford B type aortic dissection from the aortic arch to the bifurcation of the common iliac artery

This case is the first case of Stanford B type aortic dissection without acute coronary syndrome in a patient whose initial complaints was a toothache and left shoulder pain. Fortunately, the patient reported lumbago at rest — a red flag for aortic dissection — following his initial complaints, raising suspicion of this condition.

Referred pain is a term used to describe pain perceived at a site adjacent to or a distance from the site of origin.[1] As the mechanism of referred pain has not been elucidated, the taxonomy committee of the International Association for the Study of Pain has not defined this term. Several neuroanatomical and physiologic theories regarding the phenomenon of referred pain have been suggested, including the hypothesis that nociceptive dorsal horn and brainstem neurons receive convergent input signals from various tissues, thus preventing higher centers from correctly identifying the actual input source.[1] Myers suggested the simple hypothesis that thoracic disorders, such as aortic dissection, pericarditis and lung cancer, induce referred craniofacial pain via the vagus nerve.[2] Meanwhile, all cervical and thoracic cardiac rami are traced consistently to the deep cardiacplexus, which also communicates with the aorta.[3] In the thoracic region, cardiac rami arise from the T2-T6 segment of the thoracic sympathetic trunk.[3] The cervical ganglia acquire communicating branches with spinal cervical nerves and all sympathetic cardiac nerves.[4] The branches of the cervical ganglia also include the internal and external carotid nerves, sympathetic trunk and branches communicating with the glossopharyngeal nerve, pharyngeal branch of the vagus nerve, and hypoglossal nerve.[5] The presence of these communications between the aorta and somatic or pharyngeal nerves via the autonomic nervous system offers a potential explanation of the mechanism underlying the referred pain observed in this case. In addition, variability in the sympathetic pathways to the heart and/or aorta may explain the pathophysiology of this unique case.