Sanghavi, Devang K.

Glossopharyngeal neuralgia (GN) is a rare pain syndrome caused by compression of the glossopharyngeal nerve. It is typically idiopathic and often goes misdiagnosed because of its similarities to trigeminal neuralgia. Vago-glossopharyngeal neuralgia, an even rarer subset of GN, occurs when the pain is accompanied by syncope and/or arrhythmia. Here, we present the case of a 54-year-old man with oropharyngeal cancer that metastasised to areas within his left carotid sheath. He presented with numerous intermittent episodes of pain, accompanied by vagal episodes. While this presentation is similarly described in prior case reports, our case is unique in that the syndrome occurred as a direct sequelae of a metastatic tumour completely encasing the left internal carotid artery.

A 48-year-old male patient requiring extracorporeal membrane oxygenation (ECMO) support for hypoxaemic respiratory failure failed to achieve therapeutic anticoagulation with bivalirudin after continuous dose escalations, and continued to have recurrent fibrin stranding in the circuit over a 6-day course of treatment. Suspecting bivalirudin resistance, the patient was transitioned to argatroban and achieved a therapeutic response in less than 24 hours. The case describes the challenges of anticoagulation in ECMO supported patients. The interplay between bivalirudin metabolism, renal replacement therapy, and immunological effects leading to a heparin-like-effect, inflammatory mediators, and thrombotic burdens may all impact the clinical effect during bivalirudin therapy. The structural biochemistry of thrombin and bivalirudin likely plays a role in the presented patient’s successful response to argatroban. Bivalirudin may fail at achieving therapeutic anticoagulation in patients with genetic thrombin mutations or structural defects that alter the binding pockets at the thrombin exosites.

Pazopanib is a vascular endothelial growth factor receptor tyrosine kinase inhibitor (VEGFR TKI) that inhibits the vascular endothelial growth factor receptor A pathway and has the potential to cause ischaemic bowel changes, including perforation. Here we report a case of a 51-year-old man with large, metastatic, retroperitoneal leiomyosarcoma that developed a tumour-bowel fistula after 4 weeks of pazopanib therapy. He presented to the emergency department with sepsis and 1-week history of worsening fever, chills, nausea and diarrhoea. Abdominal CT findings of mesenteric and portal vein gas, commonly found in mesenteric ischaemia and VEGFR modulator-induced bowel toxicity, provided evidence for the causal relation. Unfortunately, the case was not amenable to surgery and patient succumbed to the illness.