Background: Lead is a well-known toxic metal and developmental toxin in children. Cases of systemic absorption and toxicity from lead ingestion are common. Far more unusual is lead absorption and toxicity from non-ingested lead foreign bodies (LFBs), such as bullets. When this occurs, it is most likely because the LFB is in contact with circulating fluid, such as synovial fluid and possibly cerebrospinal fluid. We describe a case of lead poisoning in an infant after gunshot injury to the head and neck with LFBs in the central nervous system (CNS). Case report: The guardian of a 5-month-old female was attempting to fix a rifle when it discharged. The bullet ricocheted and struck the girl in her neck and thorax. She was stabilized at an outside hospital and transferred to a level one pediatric trauma center. Imaging revealed extensive soft tissue shrapnel in left neck, thorax, and occipital head. There were LFBs in the spinal canal at C4 and T2. LFB also tracked into the left cerebellum, penetrating to the midline brain near the cerebral aquaduct. Initial examination showed no movement in upper extremities and withdrawal to touch in bilateral lower extremities in a stable, intubated and sedated patient. Soft tissue was tattooed with black substance; LFBs and shrapnel were present. Debridement removed visible fragments. She had a C4-5 and T2-3 laminectomy with intradural LFB removal. Post-operative imaging revealed residual LFBs in the left cerebellar hemisphere, fourth ventricle, and occipital soft tissue. Two days after injury, a capillary blood lead level (BLL) was 27 mcg/dL. Thereafter, she was able to wean from the ventilator, smile, make eye contact and regain some extremity function. Constipation occurred that was attributed to medications and critical illness. Serial BLLs went up to 50 mcg/dL at 3 weeks post-injury. Succimer was started at standard dosing. BLLs initially decreased during succimer therapy, but quickly rebounded. Using a threshold of 45 mcg/dL for chelation, she required three courses of succimer in the 6 months since her injury. Highest BLL was 59 mcg/dL. She has not developed signs of neurotoxicity, hypertension, anemia or constipation. She is meeting appropriate language and social developmental milestones with motor limited as expected from her spinal injuries. Case discussion: Any symptoms of lead toxicity in this child are complicated by her young age and her co-occurring injuries. Her BLL may have risen rapidly secondary to initial high surface area exposure. Her ongoing source of lead is likely LFBs in contact with CSF. This type of exposure may result in chronic lead toxicity and potentially greater neurotoxicity. Unfortunately, the location of these LFBs also makes removal too risky to attempt. The role that potentially higher CSF lead burden may play is unstudied. The few pediatric reports of CNS LFB include no infants and no long-term outcomes. Conclusions: Elevated blood lead levels in an infant are complicated by retained lead foreign bodies in the CNS. For this rare scenario, no precedence was found in published cases to guide chelation therapy or predict long-term outcomes.