A Patient’s Six-Month Journey From Low Sodium to Blue Toes to Stroke: Non-infective Thrombotic Endocarditis Due to Non-small Cell Lung Cancer

We report a patient's journey with a four-year history of hypertension (HTN) and hyperlipidemia (HLD), stable on beta-blocker and statin, monitored every six months by alternating visits between her cardiologist and primary care physician (PCP) in North Carolina (NC). Six months before relocating to New York (NY) she had been informed about incidental severe hyponatremia during her last outpatient visit, the need for repletion with sodium chloride tablets, and the critical importance of prompt follow-up to rule out malignancy by starting with a chest X-ray. She opted not to follow instructions, continued cigarettes, and decided to spend the summer season with her son in NY. Six months after being told of her low sodium, she presented to our NY hospital with an acute, painful right foot blue toe syndrome. During the ischemic right foot evaluation, she was discovered to have adenocarcinoma of the right lung (stage 4) and a normal transthoracic echocardiogram (TTE). Heparin was initiated and thromboembolectomy with an endovascular bovine patch to revascularize the foot was successful, and post-procedure apixaban was started. Hyponatremia was attributed to the syndrome of inappropriate antidiuretic hormone release (SIADH) secondary to non-small cell lung cancer (NSCLC). The serum sodium was stabilized, and the patient was discharged with a plan for outpatient follow-up with the cardiologist and oncologist within two weeks for hypertension, hyperlipidemia, hyponatremia, and management of stage 4 NSCLC. During her cardiology follow-up, 10 days after discharge, complaints of mild dyspnea on exertion (DOE) prompted an ECG (electrocardiogram) that revealed new T wave inversions in leads V3-6, and the patient was readmitted for non-ST elevation myocardial infarction (NSTEMI) evaluation. On day one of the readmission troponins were negative with normal ejection fraction (EF) on TTE and an acute 2 g/dl hemoglobin (Hb) drop with melena. This led to discontinuation of anticoagulation, initiation of intravenous (IV) pantoprazole, and endoscopy (EGD) which revealed gastritis. On the third day, she developed sudden expressive aphasia. Computed tomography (CT) of the head did not show any bleed but same-day magnetic resonance imaging (MRI) demonstrated multiple evolving acute infarcts. Transesophageal echocardiogram (TEE) demonstrated two large, mobile masses on the mitral valve consistent with vegetative endocarditis. Cultures for bacteria, fungi, and evaluation for organisms associated with culture-negative acute bacterial endocarditis/subacute bacterial endocarditis were unrevealing, thus confirming malignancy-associated non-infectious thrombotic endocarditis or non-bacterial thrombotic endocarditis (NBTE). Gastrointestinal (GI) bleeding ceased, and the patient initially started on a heparin drip and transitioned to enoxaparin as lifelong anticoagulation for malignancy-associated NBTE. She recovered neurologically and was given pembrolizumab. At her recent 15-month visit she continued to have no residual neurological impairments, however, new positron emission tomography (PET) detected metastasis to the liver, lung, and adrenals which prompted evaluation for hospice care. We, therefore, emphasize the need for timely diagnosis of NBTE and prompt initiation of anticoagulation in suitable patients to prevent complications such as in our patient. Additionally, hyponatremia secondary to SIADH in NSCLC is a poor prognostic indicator of overall survival.