A forty-one-year-old woman with a long history of pain in the right knee was evaluated at our institution because of acute exacerbation of this pain. Twenty-three years earlier, in Trinidad, she had been shot in both knees with a shotgun and some pellets had been removed operatively. The pellets had grazed the left knee but had directly impacted on the right knee. No fractures were noted at that time. She had chronic pain with walking and with ascending and descending stairs but needed no assistive devices (such as a cane or crutches) for walking. The pain was relieved slightly with non-steroidal anti-inflammatory medications. She had a history of occasional episodes of locking of the right knee that resolved spontaneously but no history of buckling of the knee.
Two months and ten days before she was seen by us, she had slipped, abducting the right lower extremity. However, by grabbing handrails, she had avoided a fall and prevented a direct blow to the knee. She subsequently had an increase in pain and recurrent effusion, and she was unable to walk without a cane. She went to the emergency room for evaluation (ten days before the operation).
The medical history revealed progressively severe headaches over the previous twelve years, a five-year history of transient abdominal cramps, and an intentional loss of 14.1 kilograms (thirty-one pounds) over the previous six months. The patient was taking an over-the-counter anorexic medication and had been dieting. She reported that she had no weakness, convulsions, confusion, or lethargy, and she had no history of occupational exposure to lead or consumption of substances possibly contaminated with lead. She owned no earthenware dishes or bowls.
On physical examination, the patient was found to be in moderate pain. She was alert and oriented, had no gingival gum line, and had no evidence of extensor palsy or other motor neuritis of the upper extremity. The girth of the thigh, measured ten centimeters proximal to the superior pole of the patella, was forty-five centimeters on the right and 47.5 centimeters on the left. The girth of the calf, measured ten centimeters distal to the superior patellar pole, was thirty-three centimeters on the right and 34.5 centimeters on the left. There was a healed scar, six by six centimeters, on the left thigh, at the level of the left medial femoral condyle. The right thigh also had a healed scar, four by seventeen centimeters, centered approximately three centimeters proximal to the level of the medial femoral condyle. The right knee had a large effusion, and the range of motion was 15 to 110 degrees. The motor strengths of the right hip, knee, ankle, and toe were 5 of 5. Sensation in both lower limbs was intact to light touch and pin prick. Reflexes were 2+ (strong) and equal bilaterally. The dorsalis pedis pulse was 1+ (normal) bilaterally, and the posterior tibialis pulse was trace bilaterally. Radiographs revealed multiple shotgun pellets throughout the area of the right knee (Figs. 1-A and 1-B). The serum level of lead was fifty-one micrograms per deciliter (2.46 micromoles per liter) (normal, zero to forty micrograms per deciliter [zero to 1.93 micromoles per liter]; toxic, greater than eighty micrograms per deciliter [3.86 micromoles per liter]).
Laboratory tests performed on the day of the operation revealed a hemoglobin of 121 grams per liter (normal, 120 to 160 grams per liter), a mean corpuscular volume of 70.9 cubic micrometers (normal, eighty-one to ninety-nine cubic micrometers), a mean corpuscular hemoglobin of 22.7 picograms (normal, twenty-seven to thirty-one picograms), and no basophilic stippling. The results of thyroid and liver-function tests were within normal limits, as were the levels of serum electrolytes, except for a chloride level of 106 millimoles per liter (normal, ninety-five to 105 millimoles per liter). The level of lead in the serum was fifty-seven micrograms per deciliter (2.75 micromoles per liter), the level in the urine was eighteen micrograms (0.09 micromole) per liter (normal, zero to eighty micrograms [zero to 0.39 micromole] per liter), and the level in the synovial fluid was fifteen micrograms (0.07 micromole) per liter.
The patient was taken to the operating room, and the right knee was examined arthroscopically. A shotgun pellet, four millimeters in diameter, was found in the intra-articular space and was extracted (Fig. 2). A full-thickness groove, presumably caused by the pellet, was found on the articular cartilage of the lateral femoral condyle. A chondroplasty was performed such that there were no remaining loose flaps or sharp edges (no underlying osseous surfaces were showing). Synovial hypertrophy was found, and a synovectomy was performed. Multiple foreign-body fragments were found throughout the joint (Fig. 3). The knee was irrigated copiously, and the procedure was terminated.
Biopsies revealed non-specific hyperplastic reactive synovial tissue with mild infiltration of plasma cells and lymphocytes. A granulomatous reaction to minute fragments of irregularly shaped black particulate matter was noted (Fig. 4). Specimens of cartilage taken from the lateral femoral condyle during the chondroplasty had no abnormalities.
Transmission electron microscopy demonstrated black particles, which were probably fragments of bullet (Fig. 5). Scanning electron microscopy, performed with a back-scattered electron detector, showed discrete high-density inclusions as large as 100 micrometers in diameter. A lead line scan was done; the count rate of the inclusions was consistent with that of lead, and spectral analysis showed lead peaks. The combination of these analyses proved that the inclusions in the tissue were lead.
Postoperatively, chelation therapy was begun with Succimer (2,3-dimercaptosuccinic acid), 100 milligrams given orally twice a day, and was administered for two weeks on an outpatient basis. After several weeks, the patient had complete resolution of the headaches and pain in the knee. The levels of lead in the serum decreased progressively; two months after the operation, the level was thirty-five micrograms per deciliter (1.69 micromoles per liter), and six months after the operation, it had decreased to twenty micrograms per deciliter (0.97 micromole per liter). At eighteen months, the patient reported little discomfort with walking and rare recurrence of the headaches; the level of lead was sixteen micrograms per deciliter (0.77 micromole per liter).
The signs and symptoms of early lead poisoning are often minor and non-specific and do not cause a patient to seek medical care. When medical attention is sought, the diagnosis is not obvious. Our patient was seen on the Orthopaedic Service with primary symptoms of pain, locking, and effusion of the knee and without lethargy, confusion, weakness, or anorexia related to the lead poisoning. Although the levels of lead were indeed elevated, the lead poisoning was an incidental finding and not the primary reason for the operation. Fortunately, the lead poisoning was mild and was reversible by removal of the lead pellet from the intra-articular space and chelation therapy. Our patient is at risk for possible intra-articular migration of other lead pellets and recurrence of the lead poisoning.
Exposure to lead can be commonplace, with daily dietary absorption of as much as 0.5 milligram having no detrimental effect20. Plumbism is most commonly caused by ingestion of lead-based paint by children2-4,9 or by occupational exposure, such as with painters, lead miners, and workers in battery factories20. Lead poisoning secondary to retained projectiles is rare but was reported as long ago as the ancient Roman wars3,20. The first case most commonly cited in modern medical literature was reported by Bronvin3,19,20 in 1867, although Pluskal18 might have reported one as early as 1843. The first case in the English-language literature was reported by Ellis3,19,20 in 1874. Lead toxicity may cause convulsions, somnolence, mania, delirium tremens, coma, neuritis, nausea, vomiting, abdominal cramps, anorexia, weight loss, renal insufficiency, general malaise, and death1,4,9,11,13,20,22. Orthopaedic complications include bone cysts24, localized arthropathy8,12,15-17, pseudarthrosis8, and gouty arthritis5. Serum levels of lead of as much as 920 micrograms per deciliter (44.40 micromoles per liter) have been reported following retention of lead projectiles1. The time between injury and the onset of symptoms has ranged from two days to forty years3, although patients may be asymptomatic for long periods of time3,11.
The location of the projectile in the body is a major factor in the likelihood of the development of lead intoxication. Exposure of lead to acidic synovial fluid results in greater dissolution than does exposure to human serum, water, or soft tissues1-3,7,10,14,21. A second variable that may affect the duration of the asymptomatic period is the surface area of the lead that is exposed to body tissue. Multiple small pellets have a greater surface area than one larger pellet, thus facilitating solubilization3,7. Embedded lead particles usually are not absorbed systemically because they are encapsulated by dense, avascular fibrous tissue, inhibiting their dissolution in body fluids17,18,20.
The diagnosis of lead intoxication has routinely included analysis of the levels of lead in serum and urine, as well as clinical findings. In our patient, the level of lead was elevated in the serum, urine, and synovial fluid. To confirm that the fragments that had been removed were indeed lead, intraoperative specimens were sent for definitive testing, which included scanning electron microscopy, a lead line scan, and spectral analysis. The results demonstrated conclusively that the intracellular and extracellular fragments consisted of lead. Other studies of lead intoxication have demonstrated, with use of electron microscopy, that some complexes also contain combinations of lead, calcium, and phosphorus19. Studies in which electron microscopy was used have suggested that lead is incorporated into cells to a level that causes death of cells, resulting in extracellular deposition of lead17. This suggests a need for removing lead fragments from the intra-articular space as soon as possible, to avoid localized arthropathy.
The treatment of lead intoxication has consisted primarily of chelation therapy and open techniques for removal of the fragments2,3,7,10,21-23. We believe that this is the first report of symptomatic lead poisoning treated with arthroscopic removal of lead. This technique allowed for removal of the fragments, extensive synovectomy, and débridement, without the need for an open arthrotomy. Frequently, chelation therapy is given before operative intervention to avoid sudden exacerbation of lead intoxication due to the stress of the operation11,17,22. Theoretically, lead, which is stored mostly in bone, can be released during stresses such as an operation, fever, immobilization, acidosis, and other conditions, and this would dramatically increase symptoms3,11,19,22. However, the level of lead might not increase with intervention such as the arthroscopy done in our patient.
Traditionally, chelation therapy has required hospitalization for intravenous administration. However, a new chelating agent that is given orally, Succimer, has allowed effective chelation therapy on an outpatient basis6,9. Multiple courses of chelation therapy may be needed to deplete the body stores of lead3. Chelation therapy alone may not decrease the levels of lead20. Therefore, it should be combined with operative removal of lead from the intra-articular space, and arthroscopic excision may be an effective way to achieve this goal.
NOTE: The authors gratefully acknowledge Mr. Jason Reidy for performance of the transmission electron microscopy, Mr. Tony Labissiere for performance of the x-ray microanalysis, and the medical library staff at Kingsbrook for their invaluable assistance.