Case Presentation:
A 60 year‐old man with history of tongue cancer 28 years prior and recent diagnosis of new oropharyngeal squamous cell carcinoma (T4N1M0) presented with weakness, fatigue and altered mental status. Patient was afebrile, blood pressure 114/73mmHg, tachycardic at 125/min, and oxygen saturation was 96% on 40% oxygen. On physical exam, he was cachectic with tracheostomy and gastrostomy tubes. His tongue protruded from his mouth, his neck was tense and enlarged and he had thick malodorous greenish sputum. He was alert however confused compared to baseline. Laboratory results were pertinent for WBC 58 K/uL with 22% bands and calcium 15.3mg/dL. The patient was admitted for tracheitis and hypercalcemia. He received antibiotics, fluids and calcitonin which resulted in improvement of his mental status. During his treatment, the patient had multiple syncopal episodes with hypotension and bradycardia triggered by peripheral IV insertions, bowel movements and other times without discernible stimulation. After each episode, the patient responded to IV fluid resuscitation and norepinephrine infusion. EKG and transthoracic echocardiogram were unremarkable. CT head revealed spread of the tumor around the internal carotid artery, suggestive of compression on the carotid sinus. Neurally mediated syncope (NMS) was suspected as the cause of recurrent syncope and midodrine was initiated to prevent further episodes. Initially, midodrine helped to deter further episodes but after several days, the patient continued to have recurrent syncope. We discussed treating the oropharyngeal cancer to alleviate mechanical compression on the carotid sinus. Our patient however, due to the advanced stage and overall prognosis, was unable to undergo further treatment.
Discussion:
NMS is autonomic dysregulation of postural tone resulting in hypotension, bradycardia, and loss of consciousness. Various stimuli can cause carotid‐sinus hypersensitivity, however NMS secondary to carotid sinus and baroreceptor compression by space‐occupying lesion in head and neck cancer is reported to be extremely rare with a prevalence of 0.4% of all cases of NMS. Progressive tumor growth of head and neck cancer can lead to direct compression of the internal carotid artery, and the mechanical pressure causes an increase in baroreceptor firing. Midodrine has been demonstrated to have beneficial effect in NMS and should be considered as the first‐line pharmacological agent in patients with recurrent NMS. Midodrine helps to increase the venous return, but has little effect on carotid sinus hypersensitivity, possibly explaining the refractory nature of our patient’s syncope after treatment.
Conclusions:
This case illustrates how mechanical encroachment of the internal carotid artery and carotid baroreceptors secondary to advanced head and neck cancer can lead to recurrent NMS episodes.
