A sixty-two-year-old male with a history of extensive crack cocaine use and cholecystectomy presented to the emergency department with abdominal pain, nausea, vomiting, and urobilia. The physical exam revealed moderate epigastric tenderness without scleral icterus or jaundice. The patient's total bilirubin was elevated at 5.2, and his direct bilirubin was 3.7. A computed tomography angiogram (CTA) of the abdomen and pelvis subsequently showed a 3.1 x 2.8 cm mass compressing porta hepatis. A magnetic resonance cholangiopancreatography (MRCP) showed a 4.9 x 3.0 cm mass at the porta hepatis with corresponding biliary duct obstruction at that level. An endoscopic retrograde cholangiopancreatography (ERCP) was performed with stent placement and brush biopsy, which showed predominantly benign ductal epithelium with rare, atypical cells and stenosis of the proximal common bile duct suggestive of cholangiocarcinoma. Cytology was performed on the ductal fluid and was also negative. The carbohydrate antigen (CA) 19-9 level at that time was 94.3. We discussed the possibility of performing surgery as an inpatient, but the patient had various psychosocial issues, which prompted a psychiatric evaluation. He subsequently had an internal-external biliary drain placed. The patient was discharged with plans to obtain an endoscopic ultrasound as an outpatient. He was admitted and discharged several times over the span of six months for various issues. He received an endoscopic ultrasound (EUS) at a surrounding hospital. The results were inconclusive, and a repeat EUS was recommended. On the last admission to the hospital for abdominal pain, a CT scan showed no biliary tree obstruction, which was further confirmed with an MRCP. The internal-external biliary drain was removed without recurrence of hyperbilirubinemia. We suspect that the patient's initial symptoms and radiographic findings of a biliary tree mass may have been induced by extrinsic compression secondary to lymphadenopathy caused by an adulterant used in the cutting process of abused cocaine. This is a rare occurrence that has not been described in the literature. There are associations of cocaine use to pulmonary hilar lymphadenopathy, but not biliary lymphadenopathy. We strongly suspect that this patient's obstructive jaundice and extrinsic biliary tree obstruction were caused by underlying cocaine use.