A 31-year-old male with the past medical history of spontaneous pneumothorax and hepatitis C presented to the Emergency Department with a complaint of severe, stabbing left-sided chest pain which began abruptly 4 hours prior to arrival and was worse with deep inspiration throughout the chest. He also reported that this pain was different from his previous pneumothorax chest pain. He acknowledged a non-productive cough, but denied fevers, chills or rigors. His only medication was ibuprofen 800 mg every six hours as needed.

The pertinent social history included that the patient was an active full pack per daysmoker with frequent use of marijuana. He denied IV drug use and worked as a part-time mechanic whose duties consisted of welding and grinding metal. He reported no protective equipment during these activities.

At presentation to the emergency department his initial vital signs and physical exam showed: temperature 37.9 degrees Celsius, pulse rate 96 beats per minute, blood pressure 124/83 mmHg, respiration rate 24 breaths per minute, and pulse oximetry 99% on room air. He was in apparent distress, writhing in pain, tachypneic, and he appeared disheveled and unkempt. His chest wall was non-tender to palpation, bilateral normal percussion, vocal fremitus, symmetrically clear breath sounds without crepitation or audible wheezing. His heart sounds were normal without murmur, rub or gallop. Besides multiple excoriations and a few pustules in accessible areas of his body, the rest of the patient’s physical exam was normal and unrevealing.

Initial laboratory data revealed white blood cell count of 12.1 thousand/cu mm with 62.7% neutrophils and no bandemia. The cardiac biomarkers, basic metabolic panel, coagulation studies and urinalysis were all normal. No inclusion criteria were met based on the Pulmonary Embolism Rule-Out Criteria (PERC) to warrant a d-dimer in this patient [3] .

The radiograph from his most recent emergency department discharge (Figure 1 and Figure 2) showed no acute cardiopulmonary disease and a two-view chest radiograph was performed (Figure 3 and Figure 4) which showed scattered radiopaque material between both lungs consistent with inhalation of radiopaque material. He was then admitted to the hospital.

During his hospital stay patient continued to have severe pleuritic chest pain with moderate relief from parenteral narcotics. The patient underwent a CT scan (Figures 5-9) to evaluate for thromboembolism and innumerable metallic foreign bodies were found scattered throughout each hemithorax, right ventricle and the liver which were not present in a prior study from one week before his hospital admission.

Considering his presentation and wide spread metallic microthromboemboli outside the lung tissues, inhalation of metallic objects due to unprotected welding was deemed unlikely. An intravenous metallic injection was suspected, and the Poison Control Center was contacted. A heavy metal urine toxicology collection was ordered. The following morning after urine collection, the patient’s chest pain had improved and he requested hospital discharge. He was advised to wait for urine toxicology results in order to guide therapy, but he consequently signed out against medical advice. The results returned three days later revealing urine mercury 54 ug/L (Reference range 0 - 10), urine mercury ug/day 104 (Reference range 0 - 15 ug/day) and urine mercury ug/g creatinine was 79.4 (Reference range <= 35) [4] .

Once the toxicology report had resulted, the patient was appropriate for chelation therapy to remove the mercury as the primary therapeutic intervention. He was unable to be contacted despite numerous attempts and a law enforcement visit to the patient’s last known address. Based upon historical chart review, the patient has returned to the ED with the complaint of chest pain. However, he has not shown evidence or sequelae of toxicity from his intravenous mercury exposure.

Disseminated elemental mercury microthromboembolism.