Characteristics of peripheral nerve damage caused by occupational acute trimethyltin chloride poisoning
10.11763/j.issn.2095-2619.2020.05.012
- Author:
Guilan OUYANG
1
;
Haibing ZHU
1
;
Yanwei LAI
1
;
Shanquan ZHONG
1
Author Information
1. Department of Neurology, The First Affiliated Hospital of Gannan Medical University Ganzhou, Jiangxi 341000, China
- Publication Type:Journal Article
- Keywords:
Trimethyltin chloride;
Clinial feature;
Motor nerve;
Sensory nerve;
Neuroelectrophysiology;
Deafness
- From:
China Occupational Medicine
2020;47(05):567-571
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE: To explore the characteristics of peripheral nerve injury caused by occupational acute trimethyltin chloride(TMT) poisoning. METHODS: The clinical manifestations and test data of neurotic electrophysiology, pure tone hearing threshold and acoustic immittance in 16 patients with occupational acute TMT poisoning were retrospectively analyzed. The patients were followed up after 6 months of discharge. RESULTS: Among the 16 cases of occupational acute TMT poisoning, 6, 4 and 6 cases were with mild, moderate and severe poisoning, respectively. For the firstly appeared symptoms, 7 cases had abnormal mental behavior and memory loss, 5 cases had tinnitus and hearing loss, 5 cases had decreased visual acuity, 2 cases had diplopia and 2 cases had binocular pain. The main clinical manifestations included 8 cases of disturbance of consciousness, and 6 cases of abnormal orientation and aggressive behavior. After correction of hypokalemia, 7 cases of patients had limb muscle weakness, hypomyotonia and weakened tendinous reflect, 9 cases had decreased tactile sensation below the groin in the lower limbs, and 6 cases had instability of walking. The main manifestations of neuroelectrophysiological detection were: 9 patients(accounting for 56.3%) showed abnormal neuroelectromyography, 4 cases of severe poisoning had damaged motor nerve, sensory nerve axon and myelin sheath, and the proximal nerve was also partially damaged. There were 2 cases of moderate poisoning showing abnormal symptoms, the axon and myelin sheath of sensory nerve were damaged, one common peroneal nerve was demyelinated. Three cases of mild poisoning had one common peroneal nerve axon damaged, one proximal tibial nerve damaged, and the axon and myelin sheath of sensory nerve were damaged. Brainstem auditory evoked potential I wave and visual evoked potential P100 latency prolonged and amplitude decreased in some of the patients with mild, moderate and severe poisoning. The sensorineural hearing loss occurred in 81.3% of patients. CONCLUSION: Occupational acute TMT poisoning can cause damage to motor nerve, sensory nerve axon and myelin sheath of extremities. Both distal and proximal nerves might be involved. It can also damage cochlear hair cells and optic nerve. Attention should be paid to the early treatment of peripheral nerve damage, cochlear hair cell and optic nerve damage caused by TMT.
