There are fewer than a hundred reported cases of lead toxicity from retained bullet fragments within the medical literature despite more than 475,000 nonfatal firearm related injuries in the US between 1993 and 1998. Symptoms may begin days to decades after the initial injury. Plumbism may go unrecognized until encephalopathy, with or without seizures, develops requiring admission to the Medical Intensive Care Unit (MICU). Increased lead absorption has been reported with intravertebral disc involvement, a large surface area of distribution, and osseous remodeling. We describe a case of plumbism complicated by encephalopathy and seizures from 20 year old retained bullet fragments with the aforementioned risk factors.
A 47 year-old female was transferred from an outside hospital with status epilepticus. Prior to initial presentation she reported abdominal pain, nausea, vomiting, and developed mental status changes for several months. She was diagnosed with Acute Intermittent Porphyria (AIP) and hemin therapy was initiated prior to transfer. Her status epilepticus required midazolam coma and mechanical ventilation. Repeat evaluation for porphyria was negative. Subsequently, basophilic stippling was noted on a peripheral smear. A serum lead level was markedly elevated at 111.1 μgm/dL (0.0 to 24.9 μgm/dL). Chelation therapy with Ethylene Diamine Tetra-Acetic Acid (EDTA) resulted in prompt improvement of neurological symptoms. The source for elemental lead was determined to be the 20 year old retained bullet fragments following a negative environmental evaluation of her home. Retained bullet fragments within the lateral left chest wall with surrounding osseous reaction were demonstrated on chest radiograph. Computerized tomography of the neck disclosed bullet fragments in close proximity to the carotid plexus. The bullet fragments within her chest wall were removed however those within her neck were inoperable. Maintaining a decreased serum lead level of 31 μgm/dL and improvement in her dysarthria, confusion, and abdominal pain required continued chelation treatments due to the retained bullet fragments within her neck.
Although plumbism from retained bullet fragments is rare several risk factors for increased lead absorption from bullets including intravertebral disk penetration, a large surface area of involvement, and osseous remodeling with increased osteocyte activity have been described in the medical literature. Our patient’s initial presentation and laboratory evaluation prior to transfer led us to continue treatment for porphyria. Lack of further clinical improvement directed us to reanalyze the diagnosis of AIP. Determination of her lead level resulted in appropriate therapy with rapid improvement in symptoms. Additionally, this case also illustrated the limited availability of treatment methods for persistent lead exposure from an inoperable bullet.
Prompt recognition of the risk factors for and symptoms of plumbism from bullet fragments are essential in expediting appropriate therapy including chelation in conjunction with possible surgical removal of the fragments especially when their clinical condition requires MICU admission.
F.R. Quijano, None.