To the Editor:
Motor weakness in lead poisoning commonly affects distal upper limbs. This report describes a severe lead poisoning case from retained bullet fragments, presenting with predominated proximal motor weakness, GI symptoms, anemia, and encephalopathy.
A 31-year-old male with retained bullet fragments had symptomatic lead poisoning 6 weeks after being shot by shotgun in his left chest. He developed abdominal pain and constipation without improvement with supportive care. His barium enema study was also normal. He developed muscle weakness at 10 weeks post injury. Examination at general hospital revealed proximal muscle weakness and microcytic anemia (hematocrit: 24%; mean corpuscular volume or MCV: 70 fl (80–100)) with basophilic stippling. Lead poisoning from the retained bullet fragments was suspected, and he was referred to a tertiary hospital.
On arrival at tertiary hospital, the patient was agitated and restless with generalized weakness predominate in proximal limbs; motor power grade IV in all extremities except grade III in both elbow flexion and both hips, and grade II in both shoulders. Deep tendon reflexes were absent. The physical examination was otherwise unremarkable.
Pre-chelated whole blood lead level was 126 mcg/dl (0–5). He also had transient increased thyroxine (T4) level: 2.19 ng/dl (0.70–1.48) which spontaneously resolved in one week; free T3 and thyroid stimulating hormone levels were normal. Electrolyte, creatinine, liver function, and serum creatine phosphokinase (CPK) levels were normal. A chest X-ray () and subsequent CT scan showed multiple metallic fragments in his left scapula, left upper lung, and left 4th and 5th ribs. Motor nerve conduction studies showed generalized small compound muscle action potentials (CMAP) without any change in conduction velocity, compatible with axonopathy without demyelination. Electromyography and sensory nerve study were not performed due to the patient's critical condition.
He got transfusion with packed red blood cell and was treated with dimercaprol (British anti-Lewisite or BAL) and calcium disodium ethylenediaminetetraacetic acid (EDTA). On the 4th day of chelation, the patient developed worsening encephalopathy and motor weakness despite ongoing chelation, and he was intubated for respiratory failure. Two days later, he regained his consciousness, but still had weakness with low negative inspiratory force of 3 cm H2O (< 15 suggests imminent ventilatory failure).
On the 10th day of chelation, his blood lead level had decreased to 23 mcg/dL. Dimercaprol was stopped and calcium disodium EDTA treatment was continued. After 2 weeks of chelation, his motor power started to gradually improve, first in distal musculature. Surgical debulking of the retained fragments in his lung, pleura, and ribs was performed on the 24th day. He was extubated on the 33rd day of chelation. Later, the chelator was switched to oral d-penicillamine, 750 mg/d. His clinical condition was gradually improved to totally independent active living with his blood lead level stabilized around 40 mcg/dl at the 6th month of chelation with continuing oral d-penicillamine.
Peripheral neuropathy from lead poisoning typically affects distal upper limbs.Citation1 Lead neuropathy can be due to demyelination or axonopathy. Studies in human with asymptomatic chronic lead exposure report decrease in conduction velocity compatible with demyelination, while reports of overt lead neuropathy show decreases in CMAP compatible with axonopathy.Citation1–3 Proximal muscle weakness is rare, and may be found in cases with relatively abrupt and massive lead exposure.Citation4–6 In anemic cases, more lead dissolved in plasma may readily distribute to target organs.Citation6,Citation7 In this setting, red blood cell transfusion has been recommended to bind free lead.Citation7
Even if the patient is confirmed to have severe axonopathy, we cannot exclude concomitant weakness from myopathy due to lack of electromyographic study. Hypotheses for this predominated proximal weakness are (1) rapid rising of lead levels may cause abnormal distribution and loss of selectivity to distal motor nerve, or (2) transient thyrotoxicosis may have contributed to it. Hyperthyroid-associated myopathy cases usually have normal serum CPK level and also delayed recovery of motor power.Citation8 However, this patient showed no other signs of thyrotoxicosis. Other potential causes of proximal muscle weakness, including critical illness myopathy, organophosphorus toxicity, and intermediate syndrome, were not matched with symptoms and progression of this case.
Funding
This report has no source of funding.
Declaration of interest
The authors report no declarations of interest. The authors alone are responsible for the content and writing of the paper.
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