Trichloropropane and dichlorohydrin associated with painful peripheral neurotoxicity.

Trichloropropane (TCP) and dichlorohydrin are widely used in industrial production; however, TCP and dichlorohydrin poisoning are rarely encountered in clinical practice. There have been no cases of peripheral neurotoxicity previously reported. A cluster of 23 patients who had been exposed to high levels of TCP and dichlorohydrin presented with painful peripheral neuropathy, and the pain was assessed using a visual analogue scale (VAS). Nerve conduction studies (NCS) were performed in all patients. All patients demonstrated symmetrical pin-prick pain in a stocking distribution in the lower limbs, with VAS scores between 3 and 10, with an average score of 6.8. NCS showed a mild mixture of axonal and demyelinating sensorimotor polyneuropathy in 14 of the 23 patients. After administration of standard neuropathic pain medication, pain was relieved in most patients. Painful peripheral neuropathy was the primary symptom observed in our patients, which differs from clinical and animal model reports of TCP or dichlorohydrin poisoning. However, the pathogenesis remains unidentified. TCP may be added to the list of industrial products that are toxic to the peripheral sensory nerves.

[The clinical analysis of 18 cases with acute trichloropropane poisoning].

OBJECTIVE: To summarise the clinical features of 18 cases with acute trichloropropane (TCP) poisoning for improving the diagnosis and treatment of the disease. METHODS: Exposure history, clinical manifestations, laboratorial examinations, poisoning causes and treatment were retrospectively reviewed in 18 cases with acute TCP poisoning. The results of peripheral lymphocyte micronucleus tests were compared with the healthy control group (n = 33). RESULTS: The common clinical symptoms were as following: respiratory symptoms were the earlier one set, such as chest tightness in 13, dry and sore throat in 7, cough and runny nose in 2. Gastrointestinal symptoms were more common, such as abdominal pain in 18, nausea and vomit in 14. Only 1 out of 18 patients was found with liver injury. The major manifestation was the increase in ALT and AST, which was returned to normal after treatment. ALL of the 18 patients were found TCP in their serum which concentration was from 39.0 to 310.0 ng/ml, and the average was (68.9 ± 42.1) ng/ml. The symptoms of toxic peripheral neuropathy were typical in all the patients, such as fatigue and numb limb in 18, burning pain of the distal lower limbs in 14, the symmetrical sock-like sensory dysfunction of pain, touch and vibration of the lower limbs in 13, muscle strength reduced in 7, hyporeflexia knee-jerks in 4, hyporeflexia ankle-jerks in 3. The peripheral nerve conduction velocity (NCV) examinations were as followed: the (sensore-nerve conduction velocity) SCV of peroneus super nerve in 18 and the (motor-nerve conduction velocity) MCV of tibial nerve in 8 was slowed down and the distal latency in 18 was prolonged. Micronucleus were found in all 18 cases. The micronucleus rate was 10.06‰ ± 2.80‰ and 8.24‰ ± 2.67‰ in acute TCP poisoning group and healthy control group, respectively. The difference was significant (P < 0.05). CONCLUSION: The common clinical manifestations of respiratory exposure of TCP poisoning patients were respiratory symptoms, gastrointestinal symptoms and the symptoms of toxic peripheral neuropathy. Liver injury in those 18 cases was not obvious. Lymphocyte micronucleus of peripheral blood were found in all 18 cases.