Case Presentation: A 60-year-old male patient who presented with hemoptysis 1-year prior, was found to have sub-centimeter lung nodules and multiple liver lesions on CT chest. The largest hepatic lesion on abdominal MRI was 3.2 x 1.4cm. He declined liver biopsy and presented a year later with abdominal distension, early satiety and unintentional weight loss of 30lbs. Repeat MRI abdomen now showed near replacement of the left hepatic lobe with metastases and new lesions in the right lobe. Liver biopsy showed metastatic, well-differentiated intermediate grade neuroendocrine tumor (Ki-67 proliferative rate was 5-10%) with immunohistochemistry staining positive for synaptophysin and chromogranin, negative for CDX2 and TTF-1. After 2 doses of Sandostatin, he was referred for hepatic artery embolization (HAE). The post procedural course was complicated by tachycardia, hypotension, fever (Temp 1010F), abdominal pain and confusion. Labs showed an increase in AST (86 to 1335mg/dl) and ALT (90 to 500 mg/dl), potassium of 6meq/dl, phosphate 5.5mg/dl, uric acid 10.5mg/dl and lactic acidosis. IVF resuscitation was initiated with broad spectrum antibiotics, lactulose and rifaximin for presumed hepatic encephalopathy in setting of fulminant hepatic failure. Allopurinol and rasburicase were added for tumor lysis syndrome (TLS). Blood cultures were sterile. He was admitted to ICU for management of TLS, presumed in setting of post HAE. His course was further complicated by oliguric renal failure requiring continuous renal replacement therapy and sterile ascites. By day 18 of admission, TLS, post-embolization syndrome and renal failure all resolved. He was discharged to subacute rehab and follow-up with primary oncologist.
Discussion: Neuroendocrine cancer (NEC) of unknown primary is a rare group of malignancies arising from the enterochromaffin cells with variable clinical presentations depending on the tumor differentiation or grade. Well differentiated NEC tend to derive from the gastrohepatopancreatic family of neuroendocrine tumors and have a proclivity for hepatic metastasis. HAE, employed as local therapy, may lessen the symptoms in patients with a significant hepatic burden. TLS, a rare complication of HAE, is a common oncologic emergency which may occur spontaneously or by chemotherapy-induced tumor death. The metabolic disturbances that ensue can lead to cardiac arrhythmias, acute kidney injury, seizures or death. TLS is most commonly seen in hematologic malignancies. This case describes the unusual manifestation of TLS in NEC of unknown primary following HAE; currently with few similar citations in the literature.
Conclusions: Though postembolization syndrome and fulminant hepatic failure are post procedural concerns, TLS is an uncommon manifestation in solid tumors and rare after HAE. Risk factors for TLS post HAE include large burden of hepatic metastases, rapidly dividing tumors and coincident use of nephrotoxic drugs. TLS in solid tumors must be recognized early and treated expeditiously given the high associated mortality.